Mycobacterium tuberculosis promotes arthritis development through toll-like receptor 2

Hiroya Kanagawa, Yasuo Niki, Tami Kobayashi, Yuiko Sato, Eri Katsuyama, Atsuhiro Fujie, Wu Hao, Kana Miyamoto, Toshimi Tando, Ryuichi Watanabe, Mayu Morita, Hideo Morioka, Morio Matsumoto, Yoshiaki Toyama, Takeshi Miyamoto

研究成果: Article査読

13 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)135-141
ページ数7
ジャーナルJournal of Bone and Mineral Metabolism
33
2
DOI
出版ステータスPublished - 2015 3

ASJC Scopus subject areas

  • 内分泌学、糖尿病および代謝内科学
  • 整形外科およびスポーツ医学
  • 内分泌学

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