Mycobacterium tuberculosis promotes arthritis development through toll-like receptor 2

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• 作者：Hiroya Kanagawa (1)
  Yasuo Niki (1)
  Tami Kobayashi (1)
  Yuiko Sato (1) (2)
  Eri Katsuyama (1)
  Atsuhiro Fujie (1)
  Wu Hao (1)
  Kana Miyamoto (1)
  Toshimi Tando (1)
  Ryuichi Watanabe (1)
  Mayu Morita (3)
  Hideo Morioka (1)
  Morio Matsumoto (1)
  Yoshiaki Toyama (1)
  Takeshi Miyamoto (1) (4)
  
  1. Department of Orthopaedic Surgery ; Keio University School of Medicine ; 35 Shinano-machi ; Shinjuku-ku ; Tokyo ; 160-8582 ; Japan
  2. Department of Musculoskeletal Reconstruction and Regeneration Surgery ; Keio University School of Medicine ; 35 Shinano-machi ; Shinjuku-ku ; Tokyo ; 160-8582 ; Japan
  3. Department of Dentistry and Oral Surgery ; Keio University School of Medicine ; 35 Shinano-machi ; Shinjuku-ku ; Tokyo ; 160-8582 ; Japan
  4. Department of Integrated Bone Metabolism and Immunology ; Keio University School of Medicine ; 35 Shinano-machi ; Shinjuku-ku ; Tokyo ; 160-8582 ; Japan
  
• 关键词：Mycobacterium tuberculosis ; Rheumatoid arthritis ; Toll ; like receptor 2 ; IL ; 6
• 刊名：Journal of Bone and Mineral Metabolism
• 出版年：2015
• 出版时间：March 2015
• 年：2015
• 卷：33
• 期：2
• 页码：135-141
• 全文大小：3,302 KB
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• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Metabolic Diseases
  Orthopedics
  Internal Medicine
  
• 出版者：Springer Japan
• ISSN：1435-5604

文摘

Rheumatoid arthritis (RA) is a multifactorial disease caused by genetic and environmental factors: however, precise molecular mechanisms underlying its pathogenesis remain largely unknown. Treatment of RA patients with disease-modifying biological agents occasionally promotes Mycobacterium tuberculosis infection or recurrence of M. tuberculosis, although how infection promotes arthritis has not been characterized. Here, we found that arthritis phenotypes in a collagen-induced mouse model were evident only when killed M. tuberculosis was co-administered. Treatment of cultured macrophages with killed M. tuberculosis promoted production of IL-6, a major inflammatory cytokine in RA patients, while similar treatment of TLR2-deficient macrophages failed to induce IL-6 expression. Arthritis scores, joint destruction, and serum IL-6 levels were all significantly ameliorated in TLR2-deficient compared with wild-type mice, even in animals treated with killed M. tuberculosis. These results suggest that M. tuberculosis infection enhances arthritis development and that TLR2 could serve as a therapeutic target for some forms of the disease.