2021/10/25 更新

写真a

マエカワ トモキ
前川 知樹
MAEKAWA Tomoki
所属
教育研究院 医歯学系 歯学系列 准教授
医歯学総合研究科 高度口腔機能教育研究センター 准教授
職名
准教授
外部リンク

学位

  • 博士(歯学) ( 2011年3月   新潟大学 )

研究キーワード

  • 骨代謝学

  • 抗炎症

  • 歯周治療学

  • 骨免疫学

研究分野

  • ライフサイエンス / 保存治療系歯学

経歴(researchmap)

  • 米国ペンシルベニア大学   Visiting Associate Professor (兼任)

    2019年7月 - 現在

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  • 新潟大学大学院医歯学総合研究科 高度口腔機能教育研究センター   Institute for Research Promotion   准教授(兼任)

    2019年4月 - 現在

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  • 新潟大学   新潟大学研究推進機構   研究准教授

    2016年10月 - 2019年3月

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  • 新潟大学   医歯学総合研究科 高度口腔機能教育研究センター   助教

    2015年4月 - 2019年3月

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  • 新潟大学   医歯学総合研究科 高度口腔機能教育研究センター   特任助教

    2015年3月 - 2015年4月

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  • 米国ペンシルベニア大学   リサーチアソシエート

    2013年4月 - 2015年3月

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  • 日本学術振興会 海外特別研究員

    2013年4月 - 2015年3月

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  • 米国ペンシルベニア大学   博士研究員

    2012年3月 - 2013年3月

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  • 新潟大学   大学院医歯学総合研究科 歯周診断・再建学分野   研究員

    2011年4月 - 2012年3月

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経歴

  • 新潟大学   医歯学総合研究科 高度口腔機能教育研究センター   准教授

    2019年4月 - 現在

  • 新潟大学   医歯学総合研究科 高度口腔機能教育研究センター   研究准教授

    2016年10月 - 2019年3月

  • 新潟大学   医歯学総合研究科 高度口腔機能教育研究センター   助教

    2015年4月 - 2016年10月

  • 新潟大学   医歯学総合研究科   特任助教

    2015年3月

学歴

  • 新潟大学   医歯学総合研究科   歯周診断・再建学分野

    2007年4月 - 2011年3月

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  • 新潟大学   歯学部   歯学科

    2000年4月 - 2006年3月

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所属学協会

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委員歴

  • 日本学術会議   科学者委員会 学術研究振興分科会(25期)  

    2021年7月 - 現在   

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  • 日本学術会議   歯学系委員会病態系歯学分科会連携会員 (25期)  

    2020年10月 - 現在   

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    団体区分:政府

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  • 先端歯学国際教育研究ネットワーク   委員  

    2019年4月 - 2022年3月   

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  • 日本学術会議   歯学委員会臨床系歯学分科会・連携会員 (24, 25期)  

    2017年10月 - 現在   

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    団体区分:政府

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  • 日本学術会議   若手アカデミーネットワーク分科会・幹事 (24期)  

    2017年10月 - 現在   

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    団体区分:学協会

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  • 日本学術会議   若手アカデミー会員(24, 25期)  

    2017年10月 - 現在   

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    団体区分:学協会

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  • 日本学術会議   歯学委員会基礎系歯学分科会 (24, 25期)  

    2017年10月 - 現在   

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    団体区分:政府

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留学歴

  • 米国ペンシルベニア大学   日本学術振興会海外特別研究員

    2012年3月 - 2015年3月

取得資格

  • 歯科医師

  • 日本歯周病学会認定医

 

論文

  • C3-targeted therapy in periodontal disease: moving closer to the clinic

    Hajishengallis G, Hasturk H, Lambris JD, Maekawa T, Contributing authors

    Trends in Immunoloy   2021年9月

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  • Clarithromycin inhibits pneumolysin production via downregulation of ply gene transcription despite autolysis activation 査読

    Domon H, Isono T, Hiyoshi T, Tamura H, Sasagawa K, Maekawa T, Hirayama S, Yanagihara K, Terao Y

    Microbiology Spectrum   2021年8月

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  • Effects of Erythromycin on Osteoclasts and Bone Resorption via DEL-1 Induction in Mice 査読

    Tamura H, Maekawa T, Domon H, Hiyoshi T, Hirayama S, Isono T, Sasagawa K, Yonezawa D, Takahashi N, Oda M, Maeda T, Tabeta K, Terao Y

    Antibiotics   10 ( 3 )   2021年3月

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    担当区分:責任著者   掲載種別:研究論文(学術雑誌)   出版者・発行元:MDPI AG  

    Macrolides are used to treat various infectious diseases, including periodontitis. Furthermore, macrolides are known to have immunomodulatory effects; however, the underlying mechanism of their action remains unclear. DEL-1 has emerged as an important factor in homeostatic immunity and osteoclastogenesis. Specifically, DEL-1 is downregulated in periodontitis tissues. Therefore, in the present study, we investigated whether the osteoclastogenesis inhibitory effects of erythromycin (ERM) are mediated through upregulation of DEL-1 expression. We used a ligature-induced periodontitis model in C57BL/6Ncrl wild-type or DEL-1-deficient mice and in vitro cell-based mechanistic studies to investigate how ERM inhibits alveolar bone resorption. As a result of measuring alveolar bone resorption and gene expression in the tooth ligation model, ERM treatment reduced bone loss by increasing DEL-1 expression and decreasing the expression of osteoclast-related factors in wild-type mice. In DEL-1-deficient mice, ERM failed to suppress bone loss and gene expression of osteoclast-related factors. In addition, ERM treatment downregulated osteoclast differentiation and calcium resorption in in vitro experiments with mouse bone marrow-derived macrophages. In conclusion, ERM promotes the induction of DEL-1 in periodontal tissue, which may regulate osteoclastogenesis and decrease inflammatory bone resorption. These findings suggest that ERM may exert immunomodulatory effects in a DEL-1-dependent manner.

    DOI: 10.3390/antibiotics10030312

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  • Proteolytic cleavage of HLA class II by human neutrophil elastase in pneumococcal pneumonia 査読

    Domon H, Maekawa T, Isono T, Furuta K, Kaito C, Terao Y

    Scientific Reports   2021年1月

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  • 好中球エラスターゼによる歯周炎重症化メカニズム解析と新規治療法への応用

    日吉 巧, 土門 久哲, 前川 知樹, 田村 光, 米澤 大輔, 多部田 康一, 寺尾 豊

    新潟歯学会雑誌   50 ( 2 )   115 - 115   2020年12月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

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  • 好中球エラスターゼによる歯周炎重症化メカニズム解析

    日吉 巧, 土門 久哲, 前川 知樹, 田村 光, 磯野 俊仁, 寺尾 豊, 多部田 康一

    日本歯周病学会会誌   62 ( 秋季特別 )   108 - 108   2020年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Treatment of severe pneumonia by hinokitiol in a murine antibiotic-resistant pneumococcal pneumonia model. 査読

    Isono T, Domon H, Nagai K, Maekawa T, Tamura H, Hiyoshi T, Yanagihara K, Kunitomo E, Takenaka S, Noiri Y, Terao Y

    PLOS ONE   2020年9月

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  • Erythromycin inhibits neutrophilic inflammation and mucosal disease by upregulating DEL-1. 査読

    Maekawa T, Tamura H, Domon H, Hiyoshi T, Isono T, Yonezawa D, Hayashi N, Takahashi N, Tabeta K, Maeda T, Oda M, Ziogas A, Alexaki VI, Chavakis T, Terao Y, Hajishengallis G

    JCI Insight   2020年8月

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    担当区分:筆頭著者, 責任著者  

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  • Animal model of periodontitis — Analysis of experimental ligature-induced periodontitis model in mice —. 招待 査読

    Tamura H, Maekawa T, Hiyoshi T, Terao Y

    Methods in Molecular Biology (published by Springer Nature)   2020年8月

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  • マウス歯牙結紮歯周炎モデルにおけるヒノキチオールの骨吸収抑制作用の解析

    日吉 巧, 土門 久哲, 前川 知樹, 田村 光, 米澤 大輔, 國友 栄治, 寺尾 豊, 多部田 康一

    日本歯周病学会会誌   62 ( 春季特別 )   133 - 133   2020年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • マウス歯牙結紮歯周炎モデルにおけるヒノキチオールの骨吸収抑制作用の解析

    日吉 巧, 土門 久哲, 前川 知樹, 田村 光, 米澤 大輔, 國友 栄治, 寺尾 豊, 多部田 康一

    日本歯周病学会会誌   62 ( 春季特別 )   133 - 133   2020年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Sulfated vizantin inhibits biofilm maturation by Streptococcus mutans. 査読 国際誌

    Masataka Oda, Mie Kurosawa, Hirofumi Yamamoto, Hisanori Domon, Shoji Takenaka, Tatsuya Ohsumi, Tomoki Maekawa, Naoto Yamasaki, Yui Furue, Yutaka Terao

    Microbiology and immunology   64 ( 7 )   493 - 501   2020年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Streptococcus mutans is the main pathogen of dental caries and adheres to the tooth surface via soluble and insoluble glucans produced by the bacterial glucosyltransferase enzyme. Thus, the S. mutans glucosyltransferase is an important virulence factor for this cariogenic bacterium. Sulfated vizantin effectively inhibits biofilm formation by S. mutans without affecting its growth. In this study, less S. mutans biofilm formation occurred on hydroxyapatite discs coated with sulfated vizantin than on noncoated discs. Sulfated vizantin showed no cytotoxicity against the human gingival cell line Ca9-22. Sulfated vizantin dose-dependently inhibited the extracellular release of cell-free glucosyltransferase from S. mutans and enhanced the accumulation of cell-associated glucosyltransferase, compared with that observed with untreated bacteria. Sulfated vizantin disrupted the localization balance between cell-associated glucosyltransferase and cell-free glucosyltransferase, resulting in inhibited biofilm maturation. These results indicate that sulfated vizantin can potentially serve as a novel agent for preventing dental caries.

    DOI: 10.1111/1348-0421.12797

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  • The secreted protein DEL-1 activates a β3 integrin–FAK–ERK1/2–RUNX2 pathway and promotes osteogenic differentiation and bone regeneration. 査読

    Yuh DY, Maekawa T, Li X, Kajikawa T, Bdeir K, Chavakis T, Hajishengallis G

    Journal of Biological Chemistry   295 ( 21 )   7261 - 7273   2020年4月

  • Complement C3 as a Target of Host Modulation in Periodontitis

    Hajishengallis G, Kajikawa T, Hajishengallis E, Maekawa T, Li X, Belibasakis G, Bostanci N, Mastellos DC, Yancopoulou D, Hasturk H, Lambris JD

    Emerging Therapies in Periodontics   2020年4月

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  • DHEA inhibits leukocyte recruitment through regulation of the integrin antagonist DEL-1. 査読

    Ziogas A, Maekawa T, Wiessner RJ, Le TT, Sprott D, Troullinaki M, Neuwirth A, Anastasopoulou V, Grossklaus S, Chung K, Sperandio M, Chavakis T, Hajishengallis G, Alexaki VI, co-first author

    Journal of Immunology   204 ( 5 )   1214 - 1224   2020年1月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Protective effect of hinokitiol against periodontal bone loss in ligature induced experimental periodontitis in mice. 査読

    Hiyoshi T, Domon H, Maekawa T, Yonezawa D, Kunitomo E, Tabeta K, Terao Y

    Archives of Oral Biology   2020年1月

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  • 舌ブラシ先端形状による細菌除去 および洗浄後のブラシの残留細菌数の違い 査読

    伊藤加代子, 前川知樹, 濃野 要, 井上 誠

    日摂食リハ会誌   24 ( 2 )   170 - 176   2020年1月

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  • M2 Phenotype Macrophages Colocalize with Schwann Cells in Human Dental Pulp. 査読

    Yoshiba N, Edanami N, Ohkura N, Maekawa T, Takahashi N, Tohma A, Izumi K, Maeda T, Hosoya A, Nakamura H, Tabeta K, Noiri Y, Yoshiba K

    Journal of Dental Research   2019年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • 米由来ペプチドによる炎症制御機構の検索と歯周病治療への応用研究

    田村 光, 前川 知樹, 土門 久哲, 日吉 巧, 米澤 大輔, 前田 健康, 多部田 康一, 寺尾 豊

    新潟歯学会雑誌   49 ( 2 )   82 - 82   2019年12月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

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  • Antibacterial activity of hinokitiol against both antibiotic-resistant and -susceptible pathogenic bacteria predominant in the oral cavity and upper airways. 査読

    Domon H, Hiyoshi T, Maekawa T, Yonezawa D, Tamura H, Kawabata S, Yanagihara K, Kimura O, Kunitomo E, Terao Y

    Microbiology and Immunology   63 ( 6 )   213 - 222   2019年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Aggregatibacter actinomycetemcomitansによる歯周炎重症化メカニズムの解析

    日吉 巧, 土門 久哲, 前川 知樹, 永井 康介, 田村 光, 高橋 直紀, 吉田 明弘, 寺尾 豊, 多部田 康一

    日本歯周病学会会誌   61 ( 春季特別 )   124 - 124   2019年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Aggregatibacter actinomycetemcomitans induces detachment and death of human gingival epithelial cells and fibroblasts via elastase release following leukotoxin-dependent neutrophil lysis. 査読 国際誌

    Takumi Hiyoshi, Hisanori Domon, Tomoki Maekawa, Kosuke Nagai, Hikaru Tamura, Naoki Takahashi, Daisuke Yonezawa, Tomohiro Miyoshi, Akihiro Yoshida, Koichi Tabeta, Yutaka Terao

    Microbiology and immunology   63 ( 3-4 )   100 - 110   2019年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Aggregatibacter actinomycetemcomitans is considered to be associated with periodontitis. Leukotoxin (LtxA), which destroys leukocytes in humans, is one of this bacterium's major virulence factors. Amounts of neutrophil elastase (NE), which is normally localized in the cytoplasm of neutrophils, are reportedly increased in the saliva of patients with periodontitis. However, the mechanism by which NE is released from human neutrophils and the role of NE in periodontitis is unclear. In the present study, it was hypothesized that LtxA induces NE release from human neutrophils, which subsequently causes the breakdown of periodontal tissues. LtxA-treatment did not induce significant cytotoxicity against human gingival epithelial cells (HGECs) or human gingival fibroblasts (HGFs). However, it did induce significant cytotoxicity against human neutrophils, leading to NE release. Furthermore, NE and the supernatant from LtxA-treated human neutrophils induced detachment and death of HGECs and HGFs, these effects being inhibited by administration of an NE inhibitor, sivelestat. The present results suggest that LtxA mediates human neutrophil lysis and induces the subsequent release of NE, which eventually results in detachment and death of HGECs and HGFs. Thus, LtxA-induced release of NE could cause breakdown of periodontal tissue and thereby exacerbate periodontitis.

    DOI: 10.1111/1348-0421.12672

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  • Antimicrobial susceptibility of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis clinical isolates from children with acute otitis media in Japan from 2014 to 2017. 査読 国際誌

    Kosuke Nagai, Osamu Kimura, Hisanori Domon, Tomoki Maekawa, Daisuke Yonezawa, Yutaka Terao

    Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy   25 ( 3 )   229 - 232   2019年3月

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    記述言語:英語  

    Increase in antimicrobial resistance (AMR) among pathogenic bacteria is a serious threat to public health. Surveillance studies to monitor shifting trends in resistance are important and guide the selection of appropriate antimicrobial agents for a particular organism. Furthermore, these studies help in dissemination of accurate information regarding AMR to the public. In this study, we investigated the antimicrobial susceptibility patterns of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis clinical isolates from outpatient children with acute otitis media in Japan from 2014 to 2017. A total of 8693 strains (2415 of S. pneumoniae, 3657 of H. influenzae, and 2621 of M. catarrhalis) were clinically isolated, and their antimicrobial susceptibilities to benzylpenicillin (PCG), ampicillin (ABPC), amoxicillin-clavulanic (AMPC/CVA), azithromycin (AZM), ceftriaxone (CTRX), and levofloxacin (LVFX) were investigated. Based on the minimum inhibitory concentration (MIC) breakpoints, the average proportion of S. pneumoniae isolates non-susceptible to PCG and AZM was 38.2% and 82.0% respectively. The average proportion of H. influenzae isolates non-susceptible to ABPC, CVA/AMPC, and CTRX was 61.9%, 43.5%, and 49.4%, respectively. The high prevalence of these resistant organisms is attributed to frequent use of antibiotic agents in Japan. Moreover, the proportion of LVFX-non-susceptible H. influenzae isolates increased in this four-year study. Here, we report updates regarding the AMR trends amongst the major pathogens that cause acute otitis media in Japan. Continuing surveillance of antimicrobial susceptibility and application of control measures against further transmission are required to decrease the emergence of resistant strains.

    DOI: 10.1016/j.jiac.2018.08.018

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  • Complement-Dependent Mechanisms and Interventions in Periodontal Disease. 査読

    Hajishengallis G, Kajikawa T, Hajishengallis E, Maekawa T, Reis ES, Mastellos DC, Yancopoulou D, Hasturk H, Lambris JD

    Frontiers in Immunology   10   406   2019年3月

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  • Peptides from rice endosperm protein restrain periodontal bone loss in mouse model of periodontitis. 査読 国際誌

    Hikaru Tamura, Tomoki Maekawa, Hisanori Domon, Takumi Hiyoshi, Daisuke Yonezawa, Kosuke Nagai, Akihito Ochiai, Masayuki Taniguchi, Koichi Tabeta, Takeyasu Maeda, Yutaka Terao

    Archives of oral biology   98 ( 2 )   132 - 139   2019年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    OBJECTIVE: Food-derived peptides have been reported to exhibit antibacterial activity against periodontal pathogenic bacteria. However, no effect has been shown on inflammation and bone resorption in periodontal pathology. The overall objective of the current study was to investigate how rice peptides influence biological defense mechanisms against periodontitis-induced inflammatory bone loss, and identify their novel functions as a potential anti-inflammatory drug. DESIGN: The expression of inflammatory and osteoclast-related molecules was examined in mouse macrophage-derived RAW 264.7 cell cultures using qPCR. Subsequently, the effect of these peptides on inflammatory bone loss in mouse periodontitis was examined using a mouse model of tooth ligation. Briefly, periodontal bone loss was induced for 7 days in mice by ligating the maxillary second molar and leaving the contralateral tooth un-ligated (baseline control). The mice were microinjected daily with the peptide in the gingiva until the day before euthanization. One week after the ligation, TRAP-positive multinucleated cells (MNCs) were enumerated from five random coronal sections of the ligated sites in each mouse. RESULTS: Rice peptides REP9 and REP11 significantly inhibited transcription activity of inflammatory and osteoclast-related molecules. Local treatment with the rice peptides, in mice subjected to ligature-induced periodontitis, inhibited inflammatory bone loss, explaining the decreased numbers of osteoclasts in bone tissue sections. CONCLUSION: Therefore, these data suggested that the rice peptides possess a protective effect against periodontitis.

    DOI: 10.1016/j.archoralbio.2018.11.021

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  • Immunization with pneumococcal elongation factor Tu enhances serotype-independent protection against Streptococcus pneumoniae infection. 査読 国際誌

    Kosuke Nagai, Hisanori Domon, Tomoki Maekawa, Takumi Hiyoshi, Hikaru Tamura, Daisuke Yonezawa, Rie Habuka, Akihiko Saitoh, Yutaka Terao

    Vaccine   37 ( 1 )   160 - 168   2019年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Vaccination is an effective strategy to prevent pneumococcal diseases. Currently, licensed vaccines include the pneumococcal polysaccharide vaccine (PPSV) and the pneumococcal conjugate vaccine (PCV), which target some of the most common of the 94 serotypes of S. pneumoniae based on their capsular composition. However, it has been reported that PPSV is not effective in children aged less than 2 years old and PCV induces serotype replacement, which means that the pneumococcal population has changed following widespread introduction of these vaccines, and the non-vaccine serotypes have increased in being the cause of invasive pneumococcal disease. Therefore, it is important that there is development of novel pneumococcal vaccines to either replace or complement current polysaccharide-based vaccines. Our previous study suggested that S. pneumoniae releases elongation factor Tu (EF-Tu) through autolysis followed by the induction of proinflammatory cytokines in macrophages via toll-like receptor 4, that may contribute to the development of pneumococcal diseases. In this study, we investigated the expression of EF-Tu in various S. pneumoniae strains and whether EF-Tu could be an antigen candidate for serotype-independent vaccine against pneumococcal infection. Western blotting and flow cytometry analysis revealed that EF-Tu is a common factor expressed on the surface of all pneumococcal strains tested, as well as intracellularly. In addition, we demonstrate that immunization with recombinant (r) EF-Tu induced the production of inflammatory cytokines and the IgG1 and IgG2a antibodies in mice, and increased the CD4+ T-cells proportion in splenocytes. We also reveal that anti-EF-Tu serum increased the phagocytic activity of mouse peritoneal macrophages against S. pneumoniae infection, independent of their serotypes. Finally, our results indicate that mice immunized with rEF-Tu were significantly and non-specifically protected against lethal challenges with S. pneumoniae serotypes (2 and 15A). Therefore, pneumococcal EF-Tu could be an antigen candidate for the serotype-independent vaccine against pneumococcal infection.

    DOI: 10.1016/j.vaccine.2018.11.015

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  • A bacterial metabolite ameliorates periodontal pathogen-induced gingival epithelial barrier disruption via GPR40 signaling 査読

    Miki Yamada, Naoki Takahashi, Yumi Matsuda, Keisuke Sato, Mai Yokoji, Benso Sulijaya, Tomoki Maekawa, Tatsuo Ushiki, Yoshikazu Mikami, Manabu Hayatsu, Yusuke Mizutani, Shigenobu Kishino, Jun Ogawa, Makoto Arita, Koichi Tabeta, Takeyasu Maeda, Kazuhisa Yamazaki

    Scientific Reports   8 ( 1 )   9008   2018年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Nature Publishing Group  

    Several studies have demonstrated the remarkable properties of microbiota and their metabolites in the pathogenesis of several inflammatory diseases. 10-Hydroxy-cis-12-octadecenoic acid (HYA), a bioactive metabolite generated by probiotic microorganisms during the process of fatty acid metabolism, has been studied for its protective effects against epithelial barrier impairment in the intestines. Herein, we examined the effect of HYA on gingival epithelial barrier function and its possible application for the prevention and treatment of periodontal disease. We found that GPR40, a fatty acid receptor, was expressed on gingival epithelial cells
    activation of GPR40 by HYA significantly inhibited barrier impairment induced by Porphyromonas gingivalis, a representative periodontopathic bacterium. The degradation of E-cadherin and beta-catenin, basic components of the epithelial barrier, was prevented in a GPR40-dependent manner in vitro. Oral inoculation of HYA in a mouse experimental periodontitis model suppressed the bacteria-induced degradation of E-cadherin and subsequent inflammatory cytokine production in the gingival tissue. Collectively, these results suggest that HYA exerts a protective function, through GPR40 signaling, against periodontopathic bacteria-induced gingival epithelial barrier impairment and contributes to the suppression of inflammatory responses in periodontal diseases.

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  • Mechanism of Macrolide-Induced Inhibition of Pneumolysin Release Involves Impairment of Autolysin Release in Macrolide-Resistant Streptococcus pneumoniae. 査読 国際誌

    Hisanori Domon, Tomoki Maekawa, Daisuke Yonezawa, Kosuke Nagai, Masataka Oda, Katsunori Yanagihara, Yutaka Terao

    Antimicrobial agents and chemotherapy   62 ( 11 )   2018年11月

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    記述言語:英語  

    Streptococcus pneumoniae is a leading cause of community-acquired pneumonia. Over the past 2 decades, macrolide resistance among S. pneumoniae organisms has been increasing steadily and has escalated at an alarming rate worldwide. However, the use of macrolides in the treatment of community-acquired pneumonia has been reported to be effective regardless of the antibiotic susceptibility of the causative pneumococci. Although previous studies suggested that sub-MICs of macrolides inhibit the production of the pneumococcal pore-forming toxin pneumolysin by macrolide-resistant S. pneumoniae (MRSP), the underlying mechanisms of the inhibitory effect have not been fully elucidated. Here, we show that the release of pneumococcal autolysin, which promotes cell lysis and the release of pneumolysin, was inhibited by treatment with azithromycin and erythromycin, whereas replenishing with recombinant autolysin restored the release of pneumolysin from MRSP. Additionally, macrolides significantly downregulated ply transcription followed by a slight decrease of the intracellular pneumolysin level. These findings suggest the mechanisms involved in the inhibition of pneumolysin in MRSP, which may provide an additional explanation for the benefits of macrolides on the outcome of treatment for pneumococcal diseases.

    DOI: 10.1128/AAC.00161-18

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  • 内因性抗炎症Del-1分子誘導による炎症性骨破壊の新規治療戦略

    前川 知樹, 土門 久哲, 田村 光, 日吉 巧, 寺尾 豊, 前田 健康

    日本歯周病学会会誌   60 ( 秋季特別 )   129 - 129   2018年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Gingival Exudatome Dynamics Implicate Inhibition of the Alternative Complement Pathway in the Protective Action of the C3 Inhibitor Cp40 in Nonhuman Primate Periodontitis. 査読

    Bostanci N, Bao K, Li X, Maekawa T, Grossmann J, Panse C, Briones RA, Resuello RRG, Tuplano JV, Garcia CAG, Reis ES, Lambris JD, Hajishengallis G

    Journal of Proteome Research   17 ( 9 )   3153 - 3175   2018年9月

  • 炎症および骨吸収の制御作用を有する新規食物由来ペプチドの検索

    田村 光, 前川 知樹, 土門 久哲, 永井 康介, 日吉 巧, 前田 健康, 寺尾 豊

    Journal of Oral Biosciences Supplement   2018   238 - 238   2018年9月

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    記述言語:日本語   出版者・発行元:(一社)歯科基礎医学会  

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  • Sulfated vizantin induces formation of macrophage extracellular traps 査読

    Masataka Oda, Mie Kurosawa, Hirofumi Yamamoto, Hisanori Domon, Tatsuya Kimura, Toshihito Isono, Tomoki Maekawa, Naoki Hayashi, Noriteru Yamada, Yui Furue, Daichi Kai, Yutaka Terao

    Microbiology and Immunology   62 ( 5 )   310 - 316   2018年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Blackwell Publishing Asia  

    Vizantin is an insoluble adjuvant that activates macrophages and lymphocytes. Recently, 2,2′,3,3′,4,4′-hexasulfated-vizantin (sulfated vizantin), which enables solubilization of vizantin, was developed by the present team. Sulfated vizantin was found to enhance bactericidal activity against multi-drug resistant Pseudomonas aeruginosa in RAW264.7 cells. In addition, spread of P. aeruginosa was inhibited in RAW264.7 cells treated with sulfated vizantin. When only sulfated vizantin and P. aeruginosa were incubated, sulfated vizantin did not affect growth of P. aeruginosa. Formation of DNA-based extracellular traps (ETs), a novel defense mechanism in several types of innate immune cells, helps to eliminate pathogens. In the present study, ET-forming macrophages constituted the majority of immune cells. Sulfated vizantin induced ET formation in RAW264.7 cells, whereas a Ca-chelating reagent, EDTA, and T-type calcium channel blocker, tetrandrine, inhibited ET formation and attenuated inhibition of spread of P. aeruginosa in sulfated vizantin-treated cells. Thus, sulfated vizantin induces ET formation in phagocytic cells in a Ca-dependent manner, thus preventing spread of P. aeruginosa. Hence, sulfated vizantin may be useful in the management of infectious diseases.

    DOI: 10.1111/1348-0421.12589

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  • Pneumococcal DNA-binding proteins released through autolysis induce the production of proinflammatory cytokines via toll-like receptor 4. 査読 国際誌

    Kosuke Nagai, Hisanori Domon, Tomoki Maekawa, Masataka Oda, Takumi Hiyoshi, Hikaru Tamura, Daisuke Yonezawa, Yoshiaki Arai, Mai Yokoji, Koichi Tabeta, Rie Habuka, Akihiko Saitoh, Masaya Yamaguchi, Shigetada Kawabata, Yutaka Terao

    Cellular immunology   325   14 - 22   2018年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Streptococcus pneumoniae is a leading cause of bacterial pneumonia. Our previous study suggested that S. pneumoniae autolysis-dependently releases intracellular pneumolysin, which subsequently leads to lung injury. In this study, we hypothesized that pneumococcal autolysis induces the leakage of additional intracellular molecules that could increase the pathogenicity of S. pneumoniae. Liquid chromatography tandem-mass spectrometry analysis identified that chaperone protein DnaK, elongation factor Tu (EF-Tu), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were released with pneumococcal DNA by autolysis. We demonstrated that recombinant (r) DnaK, rEF-Tu, and rGAPDH induced significantly higher levels of interleukin-6 and tumor necrosis factor production in peritoneal macrophages and THP-1-derived macrophage-like cells via toll-like receptor 4. Furthermore, the DNA-binding activity of these proteins was confirmed by surface plasmon resonance assay. We demonstrated that pneumococcal DnaK, EF-Tu, and GAPDH induced the production of proinflammatory cytokines in macrophages, and might cause host tissue damage and affect the development of pneumococcal diseases.

    DOI: 10.1016/j.cellimm.2018.01.006

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  • Neutrophil Elastase Subverts the Immune Response by Cleaving Toll-Like Receptors and Cytokines in Pneumococcal Pneumonia. 査読 国際誌

    Hisanori Domon, Kosuke Nagai, Tomoki Maekawa, Masataka Oda, Daisuke Yonezawa, Wataru Takeda, Takumi Hiyoshi, Hikaru Tamura, Masaya Yamaguchi, Shigetada Kawabata, Yutaka Terao

    Frontiers in immunology   9   732 - 732   2018年

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    記述言語:英語  

    Excessive activation of neutrophils results in the release of neutrophil elastase (NE), which leads to lung injury in severe pneumonia. Previously, we demonstrated a novel immune subversion mechanism involving microbial exploitation of this NE ability, which eventually promotes disruption of the pulmonary epithelial barrier. In the present study, we investigated the effect of NE on host innate immune response. THP-1-derived macrophages were stimulated with heat-killed Streptococcus pneumoniae or lipopolysaccharide in the presence or absence of NE followed by analysis of toll-like receptor (TLR) and cytokine expression. Additionally, the biological significance of NE was confirmed in an in vivo mouse intratracheal infection model. NE downregulated the gene transcription of multiple cytokines in THP-1-derived macrophages through the cleavage of TLRs and myeloid differentiation factor 2. Additionally, NE cleaved inflammatory cytokines and chemokines. In a mouse model of intratracheal pneumococcal challenge, administration of an NE inhibitor significantly increased proinflammatory cytokine levels in bronchoalveolar lavage fluid, enhanced bacterial clearance, and improved survival rates. Our work indicates that NE subverts the innate immune response and that inhibition of this enzyme may constitute a novel therapeutic option for the treatment of pneumococcal pneumonia.

    DOI: 10.3389/fimmu.2018.00732

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  • Secreted protein Del-1 regulates myelopoiesis in the hematopoietic stem cell niche 査読

    Ioannis Mitroulis, Lan-Sun Chen, Rashim Pal Singh, Ioannis Kourtzelis, Matina Economopoulou, Tetsuhiro Kajikawa, Maria Troullinaki, Athanasios Ziogas, Klara Ruppova, Kavita Hosur, Tomoki Maekawa, Baomei Wang, Pallavi Subramanian, Torsten Tonn, Panayotis Verginis, Malte von Bonin, Manja Wobus, Martin Bornhaeuser, Tatyana Grinenko, Marianna Di Scala, Andres Hidalgo, Ben Wielockx, George Hajishengallis, Triantafyllos Chavakis

    JOURNAL OF CLINICAL INVESTIGATION   127 ( 10 )   3624 - 3639   2017年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC CLINICAL INVESTIGATION INC  

    Hematopoietic stem cells (HSCs) remain mostly quiescent under steady-state conditions but switch to a proliferative state following hematopoietic stress, e.g., bone marrow (BM) injury, transplantation, or systemic infection and inflammation. The homeostatic balance between quiescence, self-renewal, and differentiation of HSCs is strongly dependent on their interactions with cells that constitute a specialized microanatomical environment in the BM known as the HSC niche. Here, we identified the secreted extracellular matrix protein Del-1 as a component and regulator of the HSC niche. Specifically, we found that Del-1 was expressed by several cellular components of the HSC niche, including arteriolar endothelial cells, CXCL12-abundant reticular (CAR) cells, and cells of the osteoblastic lineage. Del-1 promoted critical functions of the HSC niche, as it regulated long-term HSC (LT-HSC) proliferation and differentiation toward the myeloid lineage. Del-1 deficiency in mice resulted in reduced LT-HSC proliferation and infringed preferentially upon myelopoiesis under both steady-state and stressful conditions, such as hematopoietic cell transplantation and G-CSF-or inflammation-induced stress myelopoiesis. Del-1-induced HSC proliferation and myeloid lineage commitment were mediated by beta 3 integrin on hematopoietic progenitors. This hitherto unknown Del-1 function in the HSC niche represents a juxtacrine homeostatic adaptation of the hematopoietic system in stress myelopoiesis.

    DOI: 10.1172/JCI92571

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  • 抗炎症性分子Del-1はWnt5a-Ror2伝達経路を阻害し骨吸収を抑制する

    前川 知樹, 小林 泰浩, 土門 久哲, 永井 康介, 寺尾 豊, 前田 健康

    Journal of Oral Biosciences Supplement   2017   286 - 286   2017年9月

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    記述言語:日本語   出版者・発行元:(一社)歯科基礎医学会  

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  • Streptococcus pyogenes Phospholipase A(2) Induces the Expression of Adhesion Molecules on Human Umbilical Vein Endothelial Cells and Aorta of Mice 査読

    Masataka Oda, Hisanori Domon, Mie Kurosawa, Toshihito Isono, Tomoki Maekawa, Masaya Yamaguchi, Shigetada Kawabata, Yutaka Terao

    FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY   7   300   2017年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:FRONTIERS MEDIA SA  

    The Streptococcus pyogenes phospholipase A(2) (SIaA) gene is highly conserved in the M3 serotype of group AS. pyogenes, which often involves hypervirulent clones. However, the role of SIaA in S. pyogenes pathogenesis is unclear. Herein, we report that SIaA induces the expression of intercellular adhesion molecule 1 (ICAM1) and vascular cell adhesion molecule 1 (VCAM1) via the arachidonic acid signaling cascade. Notably, recombinant SIaA induced ICAM1 and VCAM1 expression in human umbilical vein endothelial cells (HUVECs), resulting in enhanced adhesion of human monocytic leukemia (THP-1) cells. However, Cl 34A, a variant enzyme with no enzymatic activity, did not induce such events. In addition, culture supernatants from S. pyogenes SSI-1 enhanced the adhesion of THP-1 cells to HUVECs, but culture supernatants from the AslaA isogenic mutant strain had limited effects. Aspirin, a cyclooxygenase 2 inhibitor, prevented the adhesion of THP-1 cells to HUVECs and did not induce ICAM1 and VCAM1 expression in HUVECs treated with SIaA. However, zileuton, a 5-lipoxygenase inhibitor, did not exhibit such effects. Furthermore, pre-administration of aspirin in mice intravenously injected with SIaA attenuated the transcriptional abundance of ICAM1 and VCAM1 in the aorta. These results suggested that SIaA from S. pyogenes stimulates the expression of adhesion molecules in vascular endothelial cells. Thus, SIaA contributes to the inflammation of vascular endothelial cells upon S. pyogenes infection.

    DOI: 10.3389/fcimb.2017.00300

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  • Differential Expression and Roles of Secreted Frizzled-Related Protein 5 and the Wingless Homolog Wnt5a in Periodontitis 査読

    T. Maekawa, P. Kulwattanaporn, K. Hosur, H. Domon, M. Oda, Y. Terao, T. Maeda, G. Hajishengallis

    JOURNAL OF DENTAL RESEARCH   96 ( 5 )   571 - 577   2017年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SAGE PUBLICATIONS INC  

    The Wingless/integrase-1 (Wnt) family of protein ligands and their functional antagonists, secreted frizzled-related proteins (sFRPs), regulate various biological processes ranging from embryonic development to immunity and inflammation. Wnt5a and sFRP5 comprise a typical ligand/antagonist pair, and the former molecule was recently detected at the messenger RNA (mRNA) level in human periodontitis. The main objective of this study was to investigate the interrelationship of expression of Wnt5a and sFRP5 in human periodontitis (as compared to health) and to determine their roles in inflammation and bone loss in an animal model. We detected both Wnt5a and sFRP5 mRNA in human gingiva, with Wnt5a dominating in diseased and sFRP5 in healthy tissue. Wnt5a and sFRP5 protein colocalized in the gingival epithelium, suggesting epithelial cell expression, which was confirmed in cultured human gingival epithelial cells (HGECs). The HGEC expression of Wnt5a and sFRP5 was differentially regulated by a proinflammatory stimulus (lipopolysaccharide [LPS] from Porphyromonas gingivalis) in a manner consistent with the clinical observations (i.e., LPS upregulated Wnt5a and downregulated sFRP5). In HGECs, exogenously added Wnt5a enhanced whereas sFRP5 inhibited LPS-induced inflammation, as monitored by interleukin 8 production. Consistent with this, local treatment with sFRP5 in mice subjected to ligature-induced periodontitis inhibited inflammation and bone loss, correlating with decreased numbers of osteoclasts in bone tissue sections. As in humans, mouse periodontitis was associated with high expression of Wnt5a and low expression of sFRP5, although this profile was reversed after treatment with sFRP5. In conclusion, we demonstrated a novel reciprocal relationship between sFRP5 and Wnt5a expression in periodontal health and disease, paving the way to clinical investigation of the possibility of using the Wnt5a/sFRP5 ratio as a periodontitis biomarker. Moreover, we showed that sFRP5 blocks experimental periodontal inflammation and bone loss, suggesting a promising platform for the development of a new host modulation therapy in periodontitis.

    DOI: 10.1177/0022034516687248

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  • Milk fat globule epidermal growth factor 8 inhibits periodontitis in non-human primates and its gingival crevicular fluid levels can differentiate periodontal health from disease in humans 査読

    Tetsuhiro Kajikawa, Fatimah Meshikhes, Tomoki Maekawa, Evlambia Hajishengallis, Kavita B. Hosur, Toshiharu Abe, Kevin Moss, Triantafyllos Chavakis, George Hajishengallis

    JOURNAL OF CLINICAL PERIODONTOLOGY   44 ( 5 )   472 - 483   2017年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY  

    AimWe have previously shown that the secreted glycoprotein milk fat globule epidermal growth factor 8 (MFG-E8) has anti-inflammatory and anti-osteoclastogenic properties. Our objective was to investigate the potential of MFG-E8 as a diagnostic or therapeutic agent in periodontitis.
    Materials and MethodsPeriodontitis was induced in non-human primates (NHPs) by placing ligatures around posterior teeth on both halves of the mandible for a split-mouth design: one side was treated with MFG-E8-Fc and the other with Fc control. Disease was assessed by clinical periodontal examinations, radiographic analysis of bone loss, and analysis of cytokine mRNA expression in gingival biopsy samples. Gingival crevicular fluid (GCF) was collected from human healthy volunteers or subjects with gingivitis, chronic moderate periodontitis, or chronic severe periodontitis. Additionally, GCF was collected from a subset of severe periodontitis patients following scaling and root planing (SRP) and after pocket reduction surgery. GCF was analysed to quantify MFG-E8 and periodontitis-relevant cytokines using multiplex assays.
    ResultsIn NHPs, sites treated with MFG-E8-Fc exhibited significantly less ligature-induced periodontal inflammation and bone loss than Fc control-treated sites. In humans, the GCF levels of MFG-E8 were significantly higher in health than in periodontitis, whereas the reverse was true for the proinflammatory cytokines tested. Consistently, MFG-E8 was elevated in GCF after both non-surgical (SRP) and surgical periodontal treatment of periodontitis patients.
    ConclusionMFG-E8 is, in principle, a novel therapeutic agent and biomarker of periodontitis.

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  • An ENU-induced splice site mutation of mouse Col1a1 causing recessive osteogenesis imperfecta and revealing a novel splicing rescue 査読

    Tabeta, K., Du, X., Arimatsu, K., Yokoji, M., Takahashi, N., Amizuka, N., Hasegawa, T., Crozat, K., Maekawa, T., Miyauchi, S., Matsuda, Y., Ida, T., Kaku, M., Hoebe, K., Ohno, K., Yoshie, H., Yamazaki, K., Moresco, E.M.Y., Beutler, B.

    Scientific Reports   7 ( 1 )   11717   2017年

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/s41598-017-10343-9

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  • Streptococcus pneumoniae disrupts pulmonary immune defence via elastase release following pneumolysin-dependent neutrophil lysis. 査読 国際誌

    Hisanori Domon, Masataka Oda, Tomoki Maekawa, Kosuke Nagai, Wataru Takeda, Yutaka Terao

    Scientific reports   6   38013 - 38013   2016年11月

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    記述言語:英語  

    Streptococcus pneumoniae is a leading cause of bacterial pneumonia and is the principal cause of morbidity and mortality worldwide. Previous studies suggested that excessive activation of neutrophils results in the release of neutrophil elastase, which contributes to lung injury in severe pneumonia. Although both pneumococcal virulence factors and neutrophil elastase contribute to the development and progression of pneumonia, there are no studies analysing relationships between these factors. Here, we showed that pneumolysin, a pneumococcal pore-forming toxin, induced cell lysis in primary isolated human neutrophils, leading to the release of neutrophil elastase. Pneumolysin exerted minimal cytotoxicity against alveolar epithelial cells and macrophages, whereas neutrophil elastase induced detachment of alveolar epithelial cells and impaired phagocytic activity in macrophages. Additionally, activation of neutrophil elastase did not exert bactericidal activity against S. pneumoniae in vitro. P2X7 receptor, which belongs to a family of purinergic receptors, was involved in pneumolysin-induced cell lysis. These findings suggested that infiltrated neutrophils are the primary target cells of pneumolysin, and that S. pneumoniae exploits neutrophil-elastase leakage to induce the disruption of pulmonary immune defences, thereby causing lung injury.

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  • Porphyromonas gingivalisは補体C5aとTLRを利用して免疫系から回避する

    前川 知樹, 前田 健康, 寺尾 豊

    Journal of Oral Biosciences Supplement   2016   364 - 364   2016年9月

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    記述言語:日本語   出版者・発行元:(一社)歯科基礎医学会  

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  • サル自然発症歯周炎に対する補体C3インヒビターの治療効果について

    前川 知樹, 前田 健康

    日本歯周病学会会誌   58 ( 春季特別 )   135 - 135   2016年4月

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  • Inhibition of pre-existing natural periodontitis in non-human primates by a locally administered peptide inhibitor of complement C3 査読

    Tomoki Maekawa, Ruel A. Briones, R. R. G. Resuello, Joel V. Tuplano, Evlambia Hajishengallis, Tetsuhiro Kajikawa, Sophia Koutsogiannaki, Cristina A. G. Garcia, Daniel Ricklin, John D. Lambris, George Hajishengallis

    JOURNAL OF CLINICAL PERIODONTOLOGY   43 ( 3 )   238 - 249   2016年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    AimHuman periodontitis is associated with overactivation of complement, which is triggered by different mechanisms converging on C3, the central hub of the system. We assessed whether the C3 inhibitor Cp40 inhibits naturally occurring periodontitis in non-human primates (NHPs).
    Materials and MethodsNon-human primates with chronic periodontitis were intra-gingivally injected with Cp40 either once (5 animals) or three times (10 animals) weekly for 6weeks followed by a 6-week follow-up period. Clinical periodontal examinations and collection of gingival crevicular fluid and biopsies of gingiva and bone were performed at baseline and during the study. A one-way repeated-measures anova was used for data analysis.
    ResultsWhether administered once or three times weekly, Cp40 caused a significant reduction in clinical indices that measure periodontal inflammation (gingival index and bleeding on probing), tissue destruction (probing pocket depth and clinical attachment level) or tooth mobility. These clinical changes were associated with significantly reduced levels of pro-inflammatory mediators and decreased numbers of osteoclasts in bone biopsies. The protective effects of Cp40 persisted, albeit at reduced efficacy, for at least 6weeks following drug discontinuation.
    ConclusionCp40 inhibits pre-existing chronic periodontal inflammation and osteoclastogenesis in NHPs, suggesting a novel adjunctive anti-inflammatory therapy for treating human periodontitis.

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  • 局所に投与した補体C3阻害薬による非ヒト霊長類での歯周炎の抑制(Inhibition of periodontitis in non-human primates by a locally administered complement C3 inhibitor)

    前川 知樹, 前田 健康

    日本細菌学雑誌   71 ( 1 )   95 - 95   2016年2月

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    記述言語:英語   出版者・発行元:日本細菌学会  

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  • Antagonistic effects of IL-17 and D-resolvins on endothelial Del-1 expression through a GSK-3β-C/EBPβ pathway. 査読

    Maekawa T, Hosur K, Abe T, Kantarci A, Ziogas A, Wang B, Van Dyke TE, Chavakis T, Hajishengallis G

    Nature Communications   6   8272   2015年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • DEL-1 restrains osteoclastogenesis and inhibits inflammatory bone loss in nonhuman primates 査読

    Jieun Shin, Tomoki Maekawa, Toshiharu Abe, Evlambia Hajishengallis, Kavita Hosur, Kalyani Pyaram, Ioannis Mitroulis, Triantafyllos Chavakis, George Hajishengallis

    SCIENCE TRANSLATIONAL MEDICINE   7 ( 307 )   307ra155   2015年9月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC ADVANCEMENT SCIENCE  

    DEL-1 (developmental endothelial locus-1) is an endothelial cell-secreted protein that regulates LFA-1 (lymphocyte function-associated antigen-1) integrin-dependent leukocyte recruitment and inflammation in various tissues. We identified a novel regulatory mechanism of DEL-1 in osteoclast biology. Specifically, we showed that DEL-1 is expressed by human and mouse osteoclasts and regulates their differentiation and resorptive function. Mechanistically, DEL-1 inhibited the expression of NFATc1, a master regulator of osteoclastogenesis, in a Mac-1 integrin-dependent manner. In vivo mechanistic analysis has dissociated the anti-inflammatory from the anti-bone-resorptive action of DEL-1 and identified structural components thereof mediating these distinct functions. Locally administered human DEL-1 blocked inflammatory periodontal bone loss in nonhuman primates-a relevant model of human periodontitis. The ability of DEL-1 to regulate both upstream (inflammatory cell recruitment) and downstream (osteoclastogenesis) events that lead to inflammatory bone loss paves the way to a new class of endogenous therapeutics for treating periodontitis and perhaps other inflammatory disorders.

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  • The B Cell-Stimulatory Cytokines BLyS and APRIL Are Elevated in Human Periodontitis and Are Required for B Cell-Dependent Bone Loss in Experimental Murine Periodontitis 査読

    Toshiharu Abe, Mohammed AlSarhan, Manjunatha R. Benakanakere, Tomoki Maekawa, Denis F. Kinane, Michael P. Cancro, Jonathan M. Korostoff, George Hajishengallis

    JOURNAL OF IMMUNOLOGY   195 ( 4 )   1427 - 1435   2015年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    B-lineage cells (B lymphocytes and plasma cells) predominate in the inflammatory infiltrate of human chronic periodontitis. However, their role in disease pathogenesis and the factors responsible for their persistence in chronic lesions are poorly understood. In this regard, two cytokines of the TNF ligand superfamily, a proliferation-inducing ligand (APRIL) and B-lymphocyte stimulator (BLyS), are important for the survival, proliferation, and maturation of B cells. Thus, we hypothesized that APRIL and/or BLyS are upregulated in periodontitis and contribute to induction of periodontal bone loss. This hypothesis was addressed in both human and mouse experimental systems. We show that, relative to healthy controls, the expression of APRIL and BLyS mRNA and protein was upregulated in natural and experimental periodontitis in humans and mice, respectively. The elevated expression of these cytokines correlated with increased numbers of B cells/plasma cells in both species. Moreover, APRIL and BLyS partially colocalized with kappa L chain-expressing B-lineage cells at the epithelial-connective tissue interface. Ligature-induced periodontitis resulted in significantly less bone loss in B cell-deficient mice compared with wild-type controls. Ab-mediated neutralization of APRIL or BLyS diminished the number of B cells in the gingival tissue and inhibited bone loss in wild-type, but not in B cell-deficient, mice. In conclusion, B cells and specific cytokines involved in their growth and differentiation contribute to periodontal bone loss. Moreover, APRIL and BLyS have been identified as potential therapeutic targets in periodontitis.

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  • Complement Involvement in Periodontitis: Molecular Mechanisms and Rational Therapeutic Approaches 査読

    George Hajishengallis, Tomoki Maekawa, Toshiharu Abe, Evlambia Hajishengallis, John D. Lambris

    IMMUNE RESPONSES TO BIOSURFACES: MECHANISMS AND THERAPEUTIC INTERVENTIONS   865   57 - 74   2015年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SPRINGER-VERLAG BERLIN  

    The complement system is a network of interacting fluid-phase and cell surface-associated molecules that trigger, amplify, and regulate immune and inflammatory signaling pathways. Dysregulation of this finely balanced network can destabilize host-microbe homeostasis and cause inflammatory tissue damage. Evidence from clinical and animal model-based studies suggests that complement is implicated in the pathogenesis of periodontitis, a polymicrobial community-induced chronic inflammatory disease that destroys the tooth-supporting tissues. This review discusses molecular mechanisms of complement involvement in the dysbiotic transformation of the periodontal microbiome and the resulting destructive inflammation, culminating in loss of periodontal bone support. These mechanistic studies have additionally identified potential therapeutic targets. In this regard, interventional studies in preclinical models have provided proof-of-concept for using complement inhibitors for the treatment of human periodontitis.

    DOI: 10.1007/978-3-319-18603-0_4

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  • Topical treatment with probiotic Lactobacillus brevis CD2 inhibits experimental periodontal inflammation and bone loss 査読

    T. Maekawa, G. Hajishengallis

    JOURNAL OF PERIODONTAL RESEARCH   49 ( 6 )   785 - 791   2014年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    Background and ObjectiveAn increasing body of evidence suggests that the use of probiotic bacteria is a promising intervention approach for the treatment of inflammatory diseases with a polymicrobial etiology. The objective of this study was to determine whether Lactobacillus brevis CD2 could inhibit periodontal inflammation and bone loss in experimental periodontitis.
    Material and MethodsPeriodontitis was induced by placing a silk ligature around the second maxillary molar of mice treated with L.brevis CD2 (8x10(5)CFU in 1mm(2) lyopatch) or placebo, which were placed between the gingiva and the buccal mucosa near the ligated teeth. The mice were killed after 5d and bone loss was measured morphometrically, gingival expression of proinflammatory cytokines was determined by quantitative real-time polymerase chain reaction, and CFU counts of periodontitis-associated bacteria were determined after aerobic and anaerobic culture. To determine the role of arginine deiminase released by L.brevis CD2, soluble extracts with or without formamidine (arginine deiminase inhibitor) were tested in in vitro cellular activation assays.
    ResultsMice topically treated with L.brevis CD2 displayed significantly decreased bone loss and lower expression of tumor necrosis factor, and interleukin-1, -6 and -17A as compared to placebo-treated mice. Moreover, L.brevis CD2-treated mice displayed lower counts of anaerobic bacteria but higher counts of aerobic bacteria than placebo-treated mice. In in vitro assays, the anti-inflammatory effects of soluble L.brevis CD2 extracts were heavily dependent on the presence of functional arginine deiminase, an enzyme that can inhibit nitric oxide synthesis.
    ConclusionThese data provide proof-of-concept that the probiotic L.brevis CD2 can inhibit periodontitis through modulatory effects on the host response and the periodontal microbiota.

    DOI: 10.1111/jre.12164

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  • Porphyromonas gingivalis Manipulates Complement and TLR Signaling to Uncouple Bacterial Clearance from Inflammation and Promote Dysbiosis 査読

    Tomoki Maekawa, Jennifer L. Krauss, Toshiharu Abe, Ravi Jotwani, Martha Triantafilou, Kathy Triantafilou, Ahmed Hashim, Shifra Hoch, Michael A. Curtis, Gabriel Nussbaum, John D. Lambris, George Hajishengallis

    CELL HOST & MICROBE   15 ( 6 )   768 - 778   2014年6月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:CELL PRESS  

    Certain low-abundance bacterial species, such as the periodontitis-associated oral bacterium Porphyromonas gingivalis, can subvert host immunity to remodel a normally symbiotic microbiota into a dysbiotic, disease-provoking state. However, such pathogens also exploit inflammation to thrive in dysbiotic conditions. How these bacteria evade immunity while maintaining inflammation is unclear. As previously reported, P. gingivalis remodels the oral microbiota into a dysbiotic state by exploiting complement. Now we show that in neutrophils P. gingivalis disarms a host-protective TLR2-MyD88 pathway via proteasomal degradation of MyD88, whereas it activates an alternate TLR2-Mal-PI3K pathway. This alternate TLR2-Mal-PI3K pathway blocks phagocytosis, provides "bystander'' protection to otherwise susceptible bacteria, and promotes dysbiotic inflammation in vivo. This mechanism to disengage bacterial clearance from inflammation required an intimate crosstalk between TLR2 and the complement receptor C5aR and can contribute to the persistence of microbial communities that drive dysbiotic diseases.

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  • Genetic and Intervention Studies Implicating Complement C3 as a Major Target for the Treatment of Periodontitis 査読

    Tomoki Maekawa, Toshiharu Abe, Evlambia Hajishengallis, Kavita B. Hosur, Robert A. DeAngelis, Daniel Ricklin, John D. Lambris, George Hajishengallis

    JOURNAL OF IMMUNOLOGY   192 ( 12 )   6020 - 6027   2014年6月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Chronic periodontitis is induced by a dysbiotic microbiota and leads to inflammatory destruction of tooth-supporting connective tissue and bone. The third component of complement, C3, is a point of convergence of distinct complement activation mechanisms, but its involvement in periodontitis was not previously addressed. We investigated this question using two animal species models, namely, C3-deficient or wild-type mice and nonhuman primates (NHPs) locally treated with a potent C3 inhibitor (the compstatin analog Cp40) or an inactive peptide control. In mice, C3 was required for maximal periodontal inflammation and bone loss, and for the sustenance of the dysbiotic microbiota. The effect of C3 on the microbiota was therefore different from that reported for the C5a receptor, which is required for the initial induction of dysbiosis. C3-dependent bone loss was demonstrated in distinct models, including Porphyromonas gingivalis-induced periodontitis, ligature-induced periodontitis, and aging-associated periodontitis. Importantly, local treatment of NHPs with Cp40 inhibited ligature-induced periodontal inflammation and bone loss, which correlated with lower gingival crevicular fluid levels of proinflammatory mediators (e.g., IL-17 and RANKL) and decreased osteoclastogenesis in bone biopsy specimens, as compared with control treatment. To our knowledge, this is the first time, for any disease, that complement inhibition in NHPs was shown to inhibit inflammatory processes that lead to osteoclastogenesis and bone loss. These data strongly support the feasibility of C3-targeted intervention for the treatment of human periodontitis.

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  • Role of complement in host-microbe homeostasis of the periodontium 査読

    George Hajishengallis, Toshiharu Abe, Tomoki Maekawa, Evlambia Hajishengallis, John D. Lambris

    SEMINARS IN IMMUNOLOGY   25 ( 1 )   65 - 72   2013年2月

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    記述言語:英語   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

    Complement plays a key role in immunity and inflammation through direct effects on immune cells or via crosstalk and regulation of other host signaling pathways. Deregulation of these finely balanced complement activities can link infection to inflammatory tissue damage. Periodontitis is a polymicrobial community-induced chronic inflammatory disease that can destroy the tooth-supporting tissues. In this review, we summarize and discuss evidence that complement is involved in the dysbiotic transformation of the periodontal microbiota and in the inflammatory process that leads to the destruction of periodontal bone. Recent insights into the mechanisms of complement involvement in periodontitis have additionally provided likely targets for therapeutic intervention against this oral disease. (C) 2013 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.smim.2013.04.004

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  • Relationship between serum antibody titres to Porphyromonas gingivalis and hs-CRP levels as inflammatory markers of periodontitis 査読

    Hirotaka Miyashita, Tomoyuki Honda, Tomoki Maekawa, Naoki Takahashi, Yukari Aoki, Takako Nakajima, Koichi Tabeta, Kazuhisa Yamazaki

    ARCHIVES OF ORAL BIOLOGY   57 ( 6 )   820 - 829   2012年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    Objective: The present study was designed to investigate whether titres of antibody to two strains of Porphyromonas gingivalis, FDC381 and SU63, are associated with serum high-sensitivity C-reactive protein (hs-CRP) levels in Japanese periodontitis patients.
    Design: Forty-nine patients with moderate to advanced periodontitis and 40 periodontally healthy control subjects were included in this study. hs-CRP levels and antibody titres to P. gingivalis were measured at baseline and reassessment 3-4 months after periodontal treatment in periodontitis patients as well as at the time of examination in the periodontally healthy subjects. Further, the effect of periodontal therapy, including surgical treatment and use of antibacterials on both markers, was analysed in patients.
    Results: hs-CRP levels and antibody titres to P. gingivalis were higher in periodontitis patients than in control subjects, and they significantly decreased following periodontal treatment (p < 0.005). Also, a significant decrease in hs-CRP levels as a result of periodontal treatment was found in patients with hs-CRP levels >1 mgl(-1) at baseline (p < 0.005). Probing depth, clinical attachment level, and alveolar bone loss in patients were significantly associated with a higher antibody titre to both strains of P. gingivalis (p < 0.05), but were not related to hs-CRP levels. No relationship was observed between hs-CRP levels and tertiles as defined by titres of antibody to P. gingivalis strains FDC381 and SU63.
    Conclusions: Our data indicate that hs-CRP levels were independent of antibody titres to P. gingivalis in Japanese periodontitis patients. (C) 2011 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.archoralbio.2011.11.008

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  • Oral infection with Porphyromonas gingivalis and systemic cytokine profile in C57BL/6.KOR-ApoEshl mice 査読

    S. Miyauchi, T. Maekawa, Y. Aoki, H. Miyazawa, K. Tabeta, T. Nakajima, K. Yamazaki

    JOURNAL OF PERIODONTAL RESEARCH   47 ( 3 )   402 - 408   2012年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    Background and Objective: Periodontal infection affects atherosclerotic diseases, such as coronary heart diseases. Mouse models have revealed that oral infection with Porphyromonas gingivalis induces changes in inflammatory-and lipid metabolism-related gene expression, regardless of the development of atherosclerotic lesions. However, the serum protein expression profile in the oral infection model has not been investigated. The present study aimed to analyse the effect of oral infection with P. gingivalis on the expression levels of multiple cytokines in the serum in apolipoprotein E-deficient mice by using a cytokine antibody array. Material and Methods: C57BL/ 6. KOR-Apoe shl mice were orally infected with P. gingivalis five times at 3 day intervals and were then killed. Splenocytes were isolated and analysed for proliferative activity and immunoglobulin G (IgG) production in response to in vitro restimulation with P. gingivalis. The expression levels of various cytokines in the sera were analysed using a mouse antibody array glass chip. Results: Splenocytes from P. gingivalis-infected mice demonstrated significantly greater proliferation and IgG production in response to P. gingivalis compared with those from sham-infected mice. Antibody array analysis revealed the selective upregulation of matrix metalloproteinase 3, intercellular adhesion molecule 1, insulin-like growth factor binding protein 2 and chemokine (C-X-C motif) ligand 7 and the downregulation of interleukin-17, tumor necrosis factor-a and L-selectin. Conclusion: These data demonstrate that oral infection with P. gingivalis induces alterations in systemic cytokine production. These cytokines could play roles in the development not only of periodontitis but also of atherosclerosis.

    DOI: 10.1111/j.1600-0765.2011.01441.x

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  • Porphyromonas gingivalis口腔感染による全身応答 血清中サイトカインプロファイルの変化

    宮内 小百合, 前川 知樹, 青木 由香莉, 宮沢 春菜, 多部田 康一, 中島 貴子, 山崎 和久

    新潟歯学会雑誌   42 ( 1 )   63 - 63   2012年6月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

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  • Increased expression of C-reactive protein gene in inflamed gingival tissues could be derived from endothelial cells stimulated with interleukin-6 査読

    Tomoki Maekawa, Koichi Tabeta, Keiko Kajita-Okui, Takako Nakajima, Kazuhisa Yamazaki

    ARCHIVES OF ORAL BIOLOGY   56 ( 11 )   1312 - 1318   2011年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    Background: Epidemiological studies have suggested periodontitis as a risk factor for ischemic heart disease. High sensitive C-reactive protein (hs-CRP), a predictor of cardiovascular risk, is elevated in periodontitis patients. Therefore, local infection-induced elevation of systemic CRP could account for the relationship between the 2 diseases. However, the underlying mechanism of CRP production in the periodontal tissues has not been fully elucidated. Therefore, the aim of the present study was to clarify the mechanism of CRP production in periodontal tissues.
    Methods: Gene expression of CRP in gingival biopsies was analysed by quantitative PCR. Human gingival epithelial cells (HGECs), human gingival fibroblasts (HGFBs), and human coronary artery endothelial cells (HCAECs) were characterized for CRP-producing ability by incubating with interleukin (IL)-1 beta, IL-6, soluble IL-6 receptor (sIL-6R), and Porphyromonas gingivalis strain W83.
    Results: Gene expression of CRP is significantly elevated in periodontitis lesions compared with gingivitis lesions. HCAECs, but not HGECs and HGFBs, produced CRP in response to IL-6 and IL-1 beta in the presence of sIL-6R. In contrast to IL-6, the effect of IL-1 beta on CRP production was indirect via induction of IL-6. IL-1 beta was produced by HGECs and HGFBs with stimulation of P. gingivalis antigens.
    Conclusion: These results suggest that CRP induced locally by periodontal infection may play another role in the pathogenesis of periodontal disease, and to a much lesser extent, has the potential to modulate systemic CRP level by extra-hepatic CRP production. (C) 2011 Elsevier Ltd. All rights reserved.

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  • 歯周炎罹患がPCSK9および脂質プロファイルに及ぼす影響

    宮沢 春菜, 本田 朋之, 宮内 小百合, 青木 由香莉, 宮下 博考, 高橋 直紀, 前川 知樹, 奥井 隆文, 土門 久哲, 伊藤 晴江, 中島 貴子, 多部田 康一, 山崎 和久

    日本歯周病学会会誌   53 ( 秋季特別 )   105 - 105   2011年9月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Porphyromonas gingivalis口腔感染による脂質代謝関連遺伝子の変動

    宮内 小百合, 前川 知樹, 高橋 直紀, 多部田 康一, 青木 由香莉, 宮下 博考, 宮沢 春菜, 中島 貴子, 山崎 和久

    日本歯周病学会会誌   53 ( 秋季特別 )   110 - 110   2011年9月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Porphyromonas gingivalis感染マウスモデルにおける炎症応答へのNKT細胞の関与

    青木 由香莉, 中島 貴子, 宮下 博考, 宮内 小百合, 宮沢 春菜, 高橋 直紀, 前川 知樹, 多部田 康一, 山崎 和久

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集   135回   81 - 81   2011年9月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯科保存学会  

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  • Chronic Oral Infection with Porphyromonas gingivalis Accelerates Atheroma Formation by Shifting the Lipid Profile 査読

    Tomoki Maekawa, Naoki Takahashi, Koichi Tabeta, Yukari Aoki, Hirotaka Miyashita, Sayuri Miyauchi, Haruna Miyazawa, Takako Nakajima, Kazuhisa Yamazaki

    PLOS ONE   6 ( 5 )   e20240   2011年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    Background: Recent studies have suggested that periodontal disease increases the risk of atherothrombotic disease. Atherosclerosis has been characterized as a chronic inflammatory response to cholesterol deposition in the arteries. Although several studies have suggested that certain periodontopathic bacteria accelerate atherogenesis in apolipoprotein E-deficient mice, the mechanistic link between cholesterol accumulation and periodontal infection-induced inflammation is largely unknown.
    Methodology/Principal Findings: We orally infected C57BL/6 and C57BL/6. KOR-Apoe(shl) (B6.Apoeshl) mice with Porphyromonas gingivalis, which is a representative periodontopathic bacterium, and evaluated atherogenesis, gene expression in the aorta and liver and systemic inflammatory and lipid profiles in the blood. Furthermore, the effect of lipopolysaccharide (LPS) from P. gingivalis on cholesterol transport and the related gene expression was examined in peritoneal macrophages. Alveolar bone resorption and elevation of systemic inflammatory responses were induced in both strains. Despite early changes in the expression of key genes involved in cholesterol turnover, such as liver X receptor and ATP-binding cassette A1, serum lipid profiles did not change with short-term infection. Long-term infection was associated with a reduction in serum high-density lipoprotein (HDL) cholesterol but not with the development of atherosclerotic lesions in wild-type mice. In B6.Apoeshl mice, long-term infection resulted in the elevation of very low-density lipoprotein (VLDL), LDL and total cholesterols in addition to the reduction of HDL cholesterol. This shift in the lipid profile was concomitant with a significant increase in atherosclerotic lesions. Stimulation with P. gingivalis LPS induced the change of cholesterol transport via targeting the expression of LDL receptor-related genes and resulted in the disturbance of regulatory mechanisms of the cholesterol level in macrophages.
    Conclusions/Significance: Periodontal infection itself does not cause atherosclerosis, but it accelerates it by inducing systemic inflammation and deteriorating lipid metabolism, particularly when underlying hyperlidemia or susceptibility to hyperlipidemia exists, and it may contribute to the development of coronary heart disease.

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  • Elevated Antibody Titers to Porphyromonas gingivalis as a Possible Predictor of Ischemic Vascular Disease: Results from the Tokamachi-Nakasato Cohort Study 査読

    Koichi Tabeta, Naohito Tanabe, Daisuke Yonezawa, Hirotaka Miyashita, Tomoki Maekawa, Naoki Takahashi, Takafumi Okui, Takako Nakajima, Kazuhisa Yamazaki

    JOURNAL OF ATHEROSCLEROSIS AND THROMBOSIS   18 ( 9 )   808 - 817   2011年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPAN ATHEROSCLEROSIS SOC  

    Aim: Limited epidemiological studies have investigated the relationship between ischemic vascular disease and periodontitis in non-Western populations. We investigated this relationship in a Japanese cohort by measuring serum titers of antibodies to periodontopathic bacteria.
    Methods: As part of the Tokamachi-Nakasato cohort study, we followed up 7021 participants regarding cardiovascular events over 5 years, and observed 99 ischemic vascular events: 66 cerebral infarctions and 33 cases of ischemic heart disease (IHD). For a nested case-control study, we selected 495 sex-and age-matched control subjects. Conditional logistic regression analysis was used to estimate the odds ratios (OR) and 95% confidence intervals (CI) of ischemic vascular events associated with antibody titers to Porphyromonas gingivalis FDC381 and SU63. Multivariable models were adjusted for traditional cardiovascular risk factors using propensity scores.
    Results: The highest tertile category of antibody titers to P. gingivalis FDC381 in men was significantly associated with an increased risk of cerebral infarction in only the crude model. The 2nd and 3rd tertile categories of antibody titers to P. gingivalis SU63 were significantly associated with an increased risk of cerebral infarction in men (multivariable ORs (95% CIs) were 7.12 (1.51-33.5) and 9.03 (1.97-41.5), respectively). The association was not appreciably modified when we further adjusted for serum high-sensitivity C-reactive protein levels. Antibody titers to P. gingivalis were not dose-dependently associated with the risk of IHD.
    Conclusion: High serum antibody titers to P. gingivalis SU63 could be a predictor of cerebral infarction in Japanese men independent of traditional risk factors and inflammation.

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  • Porphyromonas gingivalis長期感染マウスモデルにおける炎症、脂質代謝関連遺伝子の発現変動

    多部田 康一, 前川 知樹, 高橋 直紀, 青木 由香莉, 宮下 博考, 宮内 小百合, 奥井 隆文, 中島 貴子, 山崎 和久

    日本歯周病学会会誌   52 ( 秋季特別 )   82 - 82   2010年9月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • 動脈硬化自然発症モデルマウスにおけるPorphyromonas gingivalis長期感染後の血清脂質プロファイルの変化

    多部田 康一, 前川 知樹, 高橋 直紀, 青木 由香莉, 宮下 博考, 宮内 小百合, 奥井 隆文, 中島 貴子, 山崎 和久

    特定非営利活動法人日本歯科保存学会学術大会プログラムおよび講演抄録集   132回   44 - 44   2010年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯科保存学会  

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  • Periodontitis-associated up-regulation of systemic inflammatory mediator level may increase the risk of coronary heart disease 査読

    T. Nakajima, T. Honda, H. Domon, T. Okui, K. Kajita, H. Ito, N. Takahashi, T. Maekawa, K. Tabeta, K. Yamazaki

    JOURNAL OF PERIODONTAL RESEARCH   45 ( 1 )   116 - 122   2010年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL PUBLISHING, INC  

    Background and Objective: Although an elevation in the concentration of high-sensitivity C-reactive protein (hs-CRP) as a result of periodontal infection may account for an increased risk of developing coronary heart disease (CHD), the effect of periodontal infection on the level of hs-CRP in an otherwise healthy Japanese population has not yet been reported. The aim of the present study was to confirm, on a larger scale, our previous pilot study findings that both chronic periodontitis and subsequent periodontal treatment alter the serum levels of C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha).
    Material and Methods: The concentrations of serum hs-CRP, IL-6 and TNF-alpha were measured in 78 periodontitis patients at baseline and at re-assessment, and in 40 periodontally healthy subjects at the time of examination.
    Results: The concentrations of hs-CRP and IL-6 in the sera of periodontitis patients were significantly higher than those in control subjects. By contrast, the concentration of TNF-alpha was significantly lower in periodontitis patients than in control subjects. Whereas periodontal treatment decreased the levels of serum hs-CRP and IL-6, no such effect was observed for TNF-alpha. When the patients were subdivided into four groups according to their initial concentration of hs-CRP, only the CRP and IL-6 concentrations of the highest quartile group showed a significant reduction following periodontal treatment. No significant difference in the initial clinical parameters was observed in any quartile.
    Conclusion: Although periodontal infection does affect the concentration of hs-CRP and IL-6 in serum, a subgroup of patients exist who are highly susceptible to an increased risk of CHD associated with periodontitis, suggesting that there may be subjects who have an elevated risk of CHD independent of susceptibility to periodontal tissue destruction per se.

    DOI: 10.1111/j.1600-0765.2009.01209.x

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  • Porphyromonas gingivalis Antigens and Interleukin-6 Stimulate the Production of Monocyte Chemoattractant Protein-1 via the Upregulation of Early Growth Response-1 Transcription in Human Coronary Artery Endothelial Cells 査読

    Tomoki Maekawa, Naoki Takahashi, Tomoyuki Honda, Daisuke Yonezawa, Hirotaka Miyashita, Takafumi Okui, Koichi Tabeta, Kazuhisa Yamazaki

    JOURNAL OF VASCULAR RESEARCH   47 ( 4 )   346 - 354   2010年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:KARGER  

    Background: Individuals with periodontitis have elevated serum levels of IL-6 and C-reactive protein and have been reported to have a significantly increased risk of developing cardiovascular disease. The transcription factor early growth response factor 1 (Egr-1) has been shown to play an important role in the development and progression of atherosclerosis. However, it is not known whether periodontal infection affects the expression of Egr-1 and subsequent endothelial cells expression of monocyte chemoattractant protein (MCP)-1, a key molecule of leukocyte chemoattraction into vessels. Methods: Human coronary artery endothelial cells (HCAECs) were stimulated with either sonicated extracts from Porphyromonas gingivalis strains 381 or SU63, or a combination of IL-6 and soluble IL-6 receptor (IL-6/sIL-6R). The expression of Egr-1, and subsequently MCP-1, was then analyzed. The role of Egr-1 on MCP-1 expression was analyzed by siRNA transfection. Results: Both P. gingivalis anti-gens and IL-6/sIL-6R stimulations upregulated the expression of Egr-1, with a more robust effect by IL-6/sIL-6R. Increased expression of Egr-1 coincided with MCP-1 production, and Egr-1 downregulation by siRNA suppressed this effect. Conclusion: These results clearly suggest that periodontal infection has the potential to affect HCAECs and hence contribute to the development of subsequent atherosclerosis. Copyright (C) 2009 S. Karger AG, Basel

    DOI: 10.1159/000265568

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  • Porphyromonas gingivalis感染が冠動脈疾患リスクに及ぼす影響 歯周炎モデルマウスの病態解析

    高橋 直紀, 前川 知樹, 青木 由香莉, 宮下 博考, 奥井 隆文, 中島 貴子, 多部田 康一, 山崎 和久

    日本歯周病学会会誌   51 ( 春季特別 )   104 - 104   2009年4月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Porphyromonas gingivalis感染が冠動脈疾患リスクに及ぼす影響 感染によるマウス組織・臓器への影響

    前川 知樹, 高橋 直紀, 青木 由香莉, 宮下 博考, 奥井 隆文, 中島 貴子, 多部田 康一, 山崎 和久

    日本歯周病学会会誌   51 ( 春季特別 )   105 - 105   2009年4月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Elevated expression of IL-17 and IL-12 genes in chronic inflammatory periodontal disease 査読

    Tomoyuki Honda, Yukari Aoki, Naoki Takahashi, Tomoki Maekawa, Takako Nakajima, Harue Ito, Koichi Tabeta, Takafumi Okui, Keiko Kajita, Hisanori Domon, Kazuhisa Yamazaki

    CLINICA CHIMICA ACTA   395 ( 1-2 )   137 - 141   2008年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE BV  

    Background: A number of different theories have been postulated to explain the progression of gingivitis to periodontitis in the context of the Th1/Th2 paradigm. However, no consistent results have been obtained. Th17, a new T-cell subset producing IL-17, which is implicated in many aspect of inflammatory tissue destruction, overcomes many of the discrepant findings in the studies related to the Th1/Th2 hypothesis. We compared the gene expression profile of Th17-related molecules in gingivitis and periodontitis lesions showing distinct clinical entities.
    Methods: Gingival tissue samples were obtained from 23 gingivitis and 24 periodontitis tissues. The gene expression was measured by using quantitative real-time PCR for IL-17A, IL-17F, CCR4, CCR6, IL-12 p35 and IL-23 p19. The difference of gene expressions between gingivitis and periodontitis was analyzed by Mann-Whitney U-test. Correlations between each gene expression were also analyzed.
    Results: The expression level of IL-17A was higher than that of IL-17F and a significant difference in expression between gingivitis and periodontitis was observed only for IL-17A. CCR4 and CCR6 tended to be higher in periodontitis compared with gingivitis, although the differences were not statistically significant. Whereas the gene expression of IL-12 p35 was significantly higher in periodontitis compared with gingivitis, that of IL-23 p19 was not different between the two diseases.
    Conclusion: This study demonstrates the elevated expression of IL-17 and IL-12 in periodontitis, i.e.. the tissue destruction form of periodontal diseases, as compared with gingivitis, and provides new insight into the T-cell mediated immunopathogenesis of periodontal disease. (C) 2008 Elsevier B.V. All rights reserved.

    DOI: 10.1016/j.cca.2008.06.003

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  • 歯周炎組織におけるTh17関連サイトカイン/マーカーの遺伝子発現解析

    本田 朋之, 青木 由香莉, 高橋 直紀, 前川 知樹, 中島 貴子, 伊藤 晴江, 多部田 康一, 奥井 隆文, 梶田 桂子, 土門 久哲, 吉江 弘正, 山崎 和久

    日本歯周病学会会誌   50 ( 秋季特別 )   88 - 88   2008年9月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • 歯周疾患が脂質代謝に及ぼす影響

    中島 貴子, 本田 朋之, 奥井 隆文, 梶田 桂子, 土門 久哲, 高橋 直紀, 前川 知樹, 天沼 亮子, 伊藤 晴江, 多部田 康一, 山崎 和久

    日本歯科医師会雑誌   61 ( 5 )   551 - 551   2008年8月

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    記述言語:日本語   出版者・発行元:(公社)日本歯科医師会  

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  • 歯周炎組織における炎症性および恒常性維持ケモカインの発現バランス

    中島 貴子, 天沼 亮子, 青木 由香莉, 本田 朋之, 奥井 隆文, 土門 久哲, 梶田 桂子, 高橋 直紀, 前川 知樹, 伊藤 晴江, 多部田 康一, 山崎 和久

    日本歯科保存学雑誌   51 ( 春季特別 )   102 - 102   2008年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯科保存学会  

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  • DEL-1分子誘導による炎症性骨破壊の新規治療戦略

    前川知樹

    BIO Clinica   35 ( 7 )   2020年7月

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    担当区分:筆頭著者  

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  • 好中球エラスターゼによる歯周炎重症化メカニズム解析と新規治療法への応用

    日吉巧, 日吉巧, 土門久哲, 土門久哲, 前川知樹, 前川知樹, 前川知樹, 田村光, 田村光, 田村光, 米澤大輔, 米澤大輔, 多部田康一, 寺尾豊, 寺尾豊

    新潟歯学会雑誌   50 ( 2 )   2020年

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  • マウス歯牙結紮歯周炎モデルにおけるヒノキチオールの骨吸収抑制作用の解析

    日吉巧, 日吉巧, 土門久哲, 土門久哲, 前川知樹, 前川知樹, 前川知樹, 田村光, 田村光, 田村光, 米澤大輔, 米澤大輔, 國友栄治, 寺尾豊, 多部田康一

    日本歯周病学会会誌(Web)   62   2020年

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  • 好中球エラスターゼによる歯周炎重症化メカニズム解析

    日吉巧, 日吉巧, 土門久哲, 土門久哲, 前川知樹, 前川知樹, 前川知樹, 田村光, 田村光, 田村光, 磯野俊仁, 寺尾豊, 寺尾豊, 多部田康一

    日本歯周病学会会誌(Web)   62   2020年

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  • 米由来ペプチドによる炎症制御機構の検索と歯周病治療への応用研究

    田村 光, 前川 知樹, 土門 久哲, 日吉 巧, 米澤 大輔, 前田 健康, 多部田 康一, 寺尾 豊

    新潟歯学会雑誌   49 ( 2 )   82 - 82   2019年12月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

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  • エリスロマイシンのDel-1再誘導による炎症性骨吸収抑制効果の検証

    田村 光, 前川 知樹, 土門 久哲, 日吉 巧, 米澤 大輔, 永井 康介, 前田 健康, 寺尾 豊, 多部田 康一

    日本歯周病学会会誌   61 ( 春季特別 )   126 - 126   2019年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • エリスロマイシンのDel-1再誘導による炎症性骨吸収抑制効果の検証

    田村光, 田村光, 田村光, 前川知樹, 前川知樹, 土門久哲, 土門久哲, 日吉巧, 日吉巧, 米澤大輔, 永井康介, 前田健康, 寺尾豊, 寺尾豊, 多部田康一

    日本歯周病学会会誌(Web)   61   2019年

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  • Aggregatibacter actinomycetemcomitansによる歯周炎重症化メカニズムの解析

    日吉巧, 日吉巧, 土門久哲, 土門久哲, 前川知樹, 前川知樹, 前川知樹, 永井康介, 田村光, 田村光, 田村光, 高橋直紀, 吉田明弘, 寺尾豊, 多部田康一

    日本歯周病学会会誌(Web)   61   2019年

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  • 肺炎球菌性肺炎の病態発症メカニズムの解析と新規肺炎予防法への展開

    永井 康介, 土門 久哲, 前川 知樹, 日吉 巧, 田村 光, 米澤 大輔, 荒井 良明, 横地 麻衣, 多部田 康一, 寺尾 豊

    新潟歯学会雑誌   48 ( 1 )   57 - 58   2018年6月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

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  • 食物由来ペプチドを用いた炎症と骨吸収の制御法の検索

    田村光, 田村光, 田村光, 前川知樹, 前川知樹, 米澤大輔, 土門久哲, 土門久哲, 永井康介, 日吉巧, 日吉巧, 多部田康一, 多部田康一, 前田健康, 寺尾豊, 寺尾豊, 吉江弘正

    日本歯周病学会会誌(Web)   60   125   2018年5月

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    記述言語:日本語  

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  • Aggregatibacter actinomycetemcomitansによる歯周組織破壊メカニズムの解析

    日吉 巧, 土門 久哲, 永井 康介, 前川 知樹, 高橋 直紀, 米澤 大輔, 田村 光, 吉田 明弘, 寺尾 豊, 吉江 弘正

    日本歯周病学会会誌   60 ( 春季特別 )   128 - 128   2018年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • 食物由来ペプチドを用いた炎症と骨吸収の制御法の検索

    田村 光, 前川 知樹, 米澤 大輔, 土門 久哲, 永井 康介, 日吉 巧, 多部田 康一, 前田 健康, 寺尾 豊, 吉江 弘正

    日本歯周病学会会誌   60 ( 春季特別 )   125 - 125   2018年5月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • 抗炎症性分子Del‐1はWnt5a‐Ror2伝達経路を阻害し骨吸収を抑制する

    前川知樹, 前川知樹, 小林泰浩, 土門久哲, 土門久哲, 永井康介, 寺尾豊, 寺尾豊, 前田健康

    Journal of Oral Biosciences Supplement (Web)   2017   ROMBUNNO.P1‐20 (WEB ONLY)   2017年

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    記述言語:日本語  

    J-GLOBAL

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  • サル自然発症歯周炎に対する補体C3インヒビターの治療効果について

    前川知樹, 前田健康

    日本歯周病学会会誌(Web)   58   135   2016年4月

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    記述言語:日本語  

    J-GLOBAL

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  • Porphyromonas gingivalisは補体C5aとTLRを利用して免疫系から回避する

    前川知樹, 前田健康, 寺尾豊

    Journal of Oral Biosciences Supplement (Web)   2016   ROMBUNNO.P1‐94 (WEB ONLY)   2016年

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    記述言語:日本語  

    J-GLOBAL

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  • 歯肉組織におけるWnt5aとsFRP5の発現機能解析(Investigation of Wnt5a and sFRP5 Expressions in Healthy and Chronic Periodontitis Tissues)

    前川 知樹

    新潟歯学会雑誌   45 ( 2 )   59 - 66   2015年12月

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    記述言語:英語   出版者・発行元:新潟歯学会  

    歯周病は細菌のバイオフィルムによって引き起こされる感染症であり、宿主との免疫反応によって歯周組織の破壊と歯槽骨の吸収を引き起こす。Wnt5aは、歯周病を含む炎症反応と強い関連が報告されている。Soluble frizzled related protein-5(sFRP5)はWnt5aの受容体の相同体であり、Wnt5a経路を阻害する。歯周炎組織と健常歯肉組織においてWnt5aとsFRP5の関連性については不明な点が多い。そこで本研究では、ヒト歯肉サンプルでのWnt5aとsFRP5のmRNA発現、ヒト歯肉上皮細胞(HGECs)におけるinterleukin-8(IL-8)mRNAとケモカインのレベルを定量的PCRおよびELISAにて各々解析した。健常組織と比べて歯周病罹患組織においてWnt5a遺伝子発現は高く、sFRP5発現は抑制されていることが明らかになった。同様に、HGECsにおいてもPorphyromonas gingivalisリポ多糖によりWnt5a発現の上昇とsFRP5発現の抑制が認められた。加えて、sFRP5のHGECsにおけるIL-8の産生抑制効果が認められた。以上の事から、HGECsではWnt5aとsFRP5は双方発現し負の相関関係にあることが初めて示された。また、Wnt5aは歯周病治療の対象となること、sFPR5が歯周病治療化合物として使用可能であることが示唆された。(著者抄録)

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  • 新たな骨形成不全症モデルマウスのフェノタイプ発症機構

    多部田康一, 有松圭, 有松圭, 有松圭, 高橋直紀, 前川知樹, 宮内小百合, 宮内小百合, 宮内小百合, 山崎和久, 山崎和久

    日本歯周病学会学術大会プログラムおよび講演抄録集   55th   2012年

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  • 新たな視点から口腔疾患を誘因とする難治性疾患を考える 歯周疾患の動脈硬化症リスクに及ぼす影響

    山崎 和久, 多部田 康一, 前川 知樹, 高橋 直紀, 青木 由香莉, 宮下 博考, 宮内 小百合, 米澤 大輔, 本田 朋之, 奥井 隆文, 奥井 桂子, 伊藤 晴江, 中島 貴子

    Journal of Oral Biosciences   52 ( Suppl )   67 - 67   2010年9月

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    記述言語:日本語   出版者・発行元:(一社)歯科基礎医学会  

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  • 歯周炎患者におけるPorphyromonas gingivalisに対する抗体価と高感度CRPの関連性

    宮下 博考, 米澤 大輔, 本田 朋之, 奥井 隆文, 奥井 桂子, 前川 知樹, 高橋 直紀, 伊藤 晴江, 中島 貴子, 多部田 康一, 山崎 和久

    新潟歯学会雑誌   40 ( 1 )   98 - 98   2010年6月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

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  • 新たな骨形成不全症モデルマウスに見られた選択的スプライシング sealにおけるGT-AGルールの例外

    多部田 康一, 高橋 直紀, 前川 知樹, 山崎 和久, 網塚 憲生

    新潟歯学会雑誌   40 ( 1 )   79 - 81   2010年6月

  • ヒト歯肉上皮細胞のケモカイン産生におけるinterleukin(IL)-17の関与-IL-17受容体の発現とその機能解析-

    高橋直紀, 前川知樹, 奥井隆文, 本田朋之, 多部田康一, 中島貴子, 山崎和久

    日本歯周病学会学術大会プログラムおよび講演抄録集   53rd   2010年

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  • 歯周病原細菌は血管内皮細胞においてIL-6/sIL-6Rを介し,CRP産生を誘導する

    前川知樹, 前川知樹, 奥井桂子, 奥井桂子, 奥井隆文, 奥井隆文, 中島貴子, 中島貴子, 多部田康一, 山崎和久, 山崎和久

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   132nd   2010年

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  • 歯周炎患者におけるPorphyromonas gingivalisに対する抗体価と高感度CRPの関連性

    宮下 博考, 米澤 大輔, 本田 朋之, 奥井 隆文, 奥井 桂子[梶田], 前川 知樹, 高橋 直紀, 伊藤 晴江, 中島 貴子, 多部田 康一, 山崎 和久

    日本歯周病学会会誌   51 ( 秋季特別 )   99 - 99   2009年9月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • ORAL INFECTION OF PORPHYROMONAS GINGIVALIS INDUCES PRO-ATHEROGENIC CHANGE IN MICE

    K. Yamazaki, T. Maekawa, N. Takahashi, T. Nakajima, K. Tabeta

    ATHEROSCLEROSIS SUPPLEMENTS   10 ( 2 )   2009年6月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • 歯周炎の病態は冠動脈血管内皮細胞のEarly growth response-1発現を上昇・誘導し炎症反応を促進させる

    前川 知樹, 高橋 直紀, 本田 朋之, 宮下 博孝, 米澤 大輔, 奥井 隆文, 多部田 康一, 山崎 和久

    新潟歯学会雑誌   39 ( 1 )   86 - 86   2009年6月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

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  • Porphyromonas gingivalis感染が冠動脈疾患リスクに及ぼす影響 基本健康診査受診者における解析

    米澤 大輔, 宮下 博孝, 前川 知樹, 高橋 直紀, 青木 由香莉, 奥井 隆文, 中島 貴子, 田辺 直仁, 多部田 康一, 山崎 和久

    新潟歯学会雑誌   39 ( 1 )   87 - 87   2009年6月

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    記述言語:日本語   出版者・発行元:新潟歯学会  

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  • Porphyromonas gingivalis感染が冠動脈疾患リスクに及ぼす影響 基本健康診査受診者における解析

    米澤 大輔, 宮下 博考, 前川 知樹, 高橋 直紀, 青木 由香莉, 奥井 隆文, 中島 貴子, 田辺 直仁, 多部田 康一, 山崎 和久

    日本歯周病学会会誌   51 ( 春季特別 )   127 - 127   2009年4月

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    記述言語:日本語   出版者・発行元:(NPO)日本歯周病学会  

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  • Porphyromonas gingivalis抗原およびIL-6刺激は血管内皮細胞において転写因子Egr-1を介してMCP-1の産生を増強する

    前川知樹, 高橋直紀, 本田朋之, 宮下博考, 多部田康一, 山崎和久

    日本歯科保存学会学術大会プログラムおよび講演抄録集(Web)   131st   2009年

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  • 歯周炎マウスモデルにおける口腔内感染が血清脂質,大動脈組織の遺伝子発現変化に与える影響-歯周炎が全身に与える影響のエビデンス-

    多部田康一, 前川知樹, 高橋直紀, 梶田桂子, 奥井隆文, 土門久哲, 本田朋之, 伊藤晴江, 中島貴子, 山崎和久

    日本動脈硬化学会総会・学術集会プログラム・抄録集   40th   2008年

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講演・口頭発表等

  • DEL-1分子誘導による抗炎症および骨形成メカニズムの解明

    前川知樹

    第62回歯科基礎医学会学術大会  2020年9月 

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  • シンポジウム Keystone細菌と骨破壊の制御による歯周病の包括的な治療への挑戦 招待

    前川 知樹

    徳島大学研究クラスター講演会  2018年10月 

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    会議種別:シンポジウム・ワークショップ パネル(指名)  

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  • シンポジウム 内因性抗炎症Del-1 分子による炎症性骨破壊―歯周病とリウマチ―の治療戦略 招待

    前川 知樹

    第60回歯科基礎医学会学術大会  2018年9月 

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    記述言語:英語   会議種別:シンポジウム・ワークショップ パネル(指名)  

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  • Del1分子による歯周炎の制御メカニズム解析とサルの応用研究 招待

    前川 知樹

    第3回口腔医科学フロンティア研究会  2018年3月 

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    会議種別:口頭発表(一般)  

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  • シンポジウム 内因性Del-1分子による炎症性骨吸収の 制御メカニズム解析とサルの応用研究 招待

    前川 知樹

    第3回日本骨免疫学会ウインターセミナー  2018年1月 

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  • シンポジウム Genetic and intervention studies implicating keystone pathogens as a major target for the treatment of periodontitis 招待 国際会議

    前川 知樹

    第65回国際歯科研究学会日本部会(JADR)学術大会  2017年11月 

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    会議種別:シンポジウム・ワークショップ パネル(指名)  

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  • シンポジウム Del-1 restrains osteoclastogenesis and inhibits inflammatory bone loss in periodontitis 招待

    前川 知樹

    第59回歯科基礎医学会学術大会  2017年9月 

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  • シンポジウム 内因性Del-1分子による炎症性骨吸収の 制御メカニズム解析とサルの応用研究 招待

    前川 知樹

    第60回春季歯周病学会学術大会  2017年5月 

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    会議種別:シンポジウム・ワークショップ パネル(指名)  

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  • シンポジウム Keystone細菌と生体の相互作用 招待

    前川 知樹

    第69回日本細菌学会関西支部総会  2016年11月 

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  • シンポジウム Complement Involvement in Periodontitis: Molecular Mechanisms and Therapeutic Approaches in Mouse and Non-Human Primates Periodontitis Model 国際会議

    前川 知樹

    International Symposium on Development of Human Resources in Practical Oral Health and Treatment  2015年1月 

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    記述言語:英語   会議種別:シンポジウム・ワークショップ パネル(指名)  

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受賞

  • 学会奨励賞

    2021年10月   歯科基礎医学会  

    前川知樹

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  • 2021 Catalyst Award

    2021年10月   全米医学アカデミー(NAM)  

    Tomoki Maekawa

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  • Interstellar Initiative-Healthy Longevity Award-1st prize

    2021年3月   AMED/NYAS  

    Tomoki Maekawa

     詳細を見る

  • 日本歯周病学会学術賞

    2020年10月   日本歯周病学会  

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  • 令和2年度文部科学大臣表彰 若手科学者賞

    2020年4月   文部科学省  

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  • 2018 IADR Sigmund Socransky Young Investigator Award

    2018年7月   国際歯科研究学会  

    前川 知樹

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  • Travel Award

    2018年4月   ASBMR 2018  

    前川 知樹

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  • 奨励賞

    2018年3月   第3回口腔医科学フロンティア研究会  

    前川 知樹

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  • 岩垂育英会賞

    2017年3月   財団法人 岩垂育英会  

    前川 知樹

     詳細を見る

  • 第2回ウインターセミナー優秀演題賞

    2017年1月   日本骨免疫学会  

    前川 知樹

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  • 日本歯周病学会奨励賞

    2016年5月   日本歯周病学会  

    前川 知樹

     詳細を見る

  • 新潟大学学長賞

    2015年7月   新潟大学  

    前川 知樹

     詳細を見る

  • Young investigator award

    2014年6月   International Conference on Complement Therapeutics  

    前川 知樹

     詳細を見る

  • 日本歯科保存学会奨励賞

    2011年3月   日本歯科保存学会  

    前川 知樹

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共同研究・競争的資金等の研究

  • DEL-1分子による免疫調節および骨再生賦活化メカニズム解明

    2020年12月 - 2022年3月

    テルモ生命科学振興財団  研究開発助成 

    前川 知樹

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  • DEL-1分子による抗炎症と再生賦活化機構の解明

    2020年12月 - 2022年3月

    興和生命科学振興財団  研究助成 

    前川 知樹

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    担当区分:研究代表者 

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  • The correlation of ectopic calcification signatures in the ageing eye and cardiovascular system

    2020年9月 - 2022年4月

    国立研究開発法人日本医療研究開発機構(AMED)  医療分野国際科学技術共同研究開発推進事業-Interstellar Initiative 

    前川 知樹

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    担当区分:研究代表者 

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  • 恒常性維持タンパク質DEL-1の自律的誘導法による抗炎症不活化機構の解明

    2020年8月 - 2022年3月

    武田科学振興財団  医学系研究助成(基礎) 

    前川 知樹

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  • DEL-1が繋ぐ口腔の細胞間ネットワーク機構解明

    2020年7月 - 2022年3月

    公益財団法人 上原記念生命科学財団  研究奨励金 

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    担当区分:研究代表者 

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  • 肺炎重症化因子のプロテオーム解析を基盤とする創薬研究への展開

    2020年4月

    日本学術振興会  基盤研究(C) 

    土門 久哲, 分担者, 前川 知樹

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    担当区分:研究分担者 

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  • 薬剤耐性肺炎球菌のin vivo MS解析とキューブ型DNA抗菌薬の開発研究

    2020年4月

    日本学術振興会  基盤研究(B) 

    寺尾 豊,分担者,前川 知樹

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    担当区分:研究分担者 

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  • MRSAを特異標的とするCRISPR-Cas型抗菌薬の開発研究

    2020年4月

    日本学術振興会  挑戦的(萌芽) 

    寺尾 豊,分担者,前川 知樹

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    担当区分:研究分担者 

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  • 炎症の進展と寛解に関与する好中球サブセット同定への挑戦

    2019年6月 - 2021年3月

    日本学術振興会  挑戦的研究(萌芽) 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • 内因性抗炎症Del-1分子の誘導による炎症性骨破壊の新規治療戦略

    2019年4月 - 2022年3月

    日本学術振興会  基盤研究(B) 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • 内因性抗炎症分子の自律的誘導による炎症性骨破壊治療への挑戦

    2019年3月 - 2020年3月

    公益財団法人 千里ライフサイエンス振興財団  2018年度 岸本基金研究助成 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • 内因性Del-1分子による骨代謝と炎症制御の統合的理解

    2018年6月 - 2021年3月

    日本学術振興会  国際共同研究加速基金(国際共同研究強化) 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • MRSA特異的な3D転換性DNAアプタマー型抗菌薬の構築と開発技術の確立研究

    2018年4月 - 2020年3月

    日本学術振興会  挑戦的研究(萌芽) 

    寺尾 豊, 分担者, 前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • 大規模菌叢解析データを用いた歯周病治療法の最適化クリティカルパスの開発

    2017年7月 - 2019年3月

    日本学術振興会  挑戦的研究(萌芽) 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • 好中球免疫を利用した肺炎球菌の肺炎重症化メカニズムと制御法の分子検索

    2017年4月 - 2020年3月

    日本学術振興会  基盤研究(B) 

    寺尾 豊, 分担者, 前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • Keystone細菌制御による新しい歯周病治療法の開発

    2017年4月 - 2018年3月

    日本歯周病学会  シーズ育成若手奨励研究助成 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • 老化により減少する内因性抗炎症因子の再誘導による生体恒常性維持機構の解明

    2017年4月 - 2018年3月

    中島国際記念交流財団  日本人若手研究者研究助成金 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • 内因性Del-1分子に着目した炎症制御のメカニズム解析と応用研究

    2016年4月 - 2019年3月

    日本学術振興会  若手研究(A) 

    前川 知樹

      詳細を見る

    担当区分:研究代表者  資金種別:競争的資金

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  • コメ由来プロテアーゼ阻害剤を用いた誤嚥性肺炎重症化制御法の検索

    2016年4月 - 2018年3月

    日本学術振興会  挑戦的萌研究 

    寺尾 豊, 分担者, 前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • Del-1の分子メカニズム解析に基づくKeystone細菌制御

    2015年8月 - 2017年3月

    日本学術振興会  研究活動スタート支援 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • 補体拮抗薬を用いた新規歯周病治療法の確立

    2015年8月 - 2016年3月

    新潟大学  平成27年度新潟大学若手教員研究奨励費 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • Del-1の分子メカニズム解析と歯周炎治療への応用

    2015年7月 - 2017年3月

    武田科学振興財団  医学研究奨励賞(感染症分野) 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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  • プロバイオティクスを応用した新規歯周病治療法の開発

    2013年4月 - 2015年3月

    日本学術振興会  海外特別研究員 

    前川 知樹

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    担当区分:研究代表者  資金種別:競争的資金

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担当経験のある授業科目(researchmap)

  • 免疫学

    機関名:新潟大学

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  • 口腔細菌学

    機関名:新潟大学

     詳細を見る

  • 細菌学

    機関名:新潟大学

     詳細を見る

  • 微生物学

    機関名:新潟大学

     詳細を見る

担当経験のある授業科目

  • 微生物学Ⅰ

    2017年
    -
    2019年
    機関名:新潟大学

  • 微生物学Ⅱ

    2017年
    -
    2018年
    機関名:新潟大学

  • 歯学研究演習

    2017年
    -
    2018年
    機関名:新潟大学

  • 微生物学Ⅰ・Ⅱ

    2016年
    -
    2017年
    機関名:新潟大学

  • 基礎科学演習

    2015年
    -
    2016年
    機関名:新潟大学