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

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)135-141
Number of pages7
JournalJournal of Bone and Mineral Metabolism
Volume33
Issue number2
DOIs
Publication statusPublished - 2015 Jan 1

Keywords

  • IL-6
  • Mycobacterium tuberculosis
  • Rheumatoid arthritis
  • Toll-like receptor 2

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Orthopedics and Sports Medicine
  • Endocrinology

Fingerprint Dive into the research topics of 'Mycobacterium tuberculosis promotes arthritis development through toll-like receptor 2'. Together they form a unique fingerprint.

  • Cite this

    Kanagawa, H., Niki, Y., Kobayashi, T., Sato, Y., Katsuyama, E., Fujie, A., Hao, W., Miyamoto, K., Tando, T., Watanabe, R., Morita, M., Morioka, H., Matsumoto, M., Toyama, Y., & Miyamoto, T. (2015). Mycobacterium tuberculosis promotes arthritis development through toll-like receptor 2. Journal of Bone and Mineral Metabolism, 33(2), 135-141. https://doi.org/10.1007/s00774-014-0575-9