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Mycobacterium tuberculosis promotes arthritis development through Toll-like receptor 2
Hiroya Kanagawa1, Yasuo Niki, Tami Kobayashi
1Department of Orthopaedic Surgery, Keio University School of Medicine, 35 Shinano-machi, Shinjuku-ku, Tokyo, 160-8582, Japan.
Journal of Bone and Mineral Metabolism
|March 18, 2014
Summary
Mycobacterium tuberculosis infection exacerbates rheumatoid arthritis (RA) development in mice. Toll-like receptor 2 (TLR2) activation by M. tuberculosis drives IL-6 production, a key factor in RA pathogenesis.
Area of Science:
- Immunology
- Rheumatology
- Microbiology
Background:
- Rheumatoid arthritis (RA) pathogenesis involves genetic and environmental factors, with precise molecular mechanisms remaining unclear.
- Biological agents for RA can trigger Mycobacterium tuberculosis (M. tuberculosis) infections, but the link to arthritis promotion is not well understood.
Purpose of the Study:
- To investigate the role of M. tuberculosis in exacerbating arthritis.
- To elucidate the molecular mechanisms, specifically the involvement of Toll-like receptor 2 (TLR2), in M. tuberculosis-induced arthritis.
Main Methods:
- A collagen-induced mouse model of arthritis was used.
- Mice were co-administered killed M. tuberculosis.
- Macrophage cultures and TLR2-deficient mice were utilized to assess IL-6 production and arthritis severity.
Main Results:
- Arthritis phenotypes were observed only when killed M. tuberculosis was co-administered.
- Killed M. tuberculosis induced IL-6 production in macrophages, dependent on TLR2.
- TLR2 deficiency significantly ameliorated arthritis scores, joint destruction, and serum IL-6 levels.
Conclusions:
- M. tuberculosis infection enhances arthritis development.
- TLR2 plays a critical role in mediating M. tuberculosis-induced inflammation in arthritis.
- TLR2 represents a potential therapeutic target for RA associated with M. tuberculosis.
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