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KMID : 0923620140140010038
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Immune Network
2014 Volume.14 No. 1 p.38 ~ p.44
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Gut-residing Microbes Alter the Host Susceptibility to Autoantibody-mediated Arthritis
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Lee Hye-Rim
Jin Bo-Eun
Jang Eun-Kyeong
Lee A-Reum
Han Dong-Soo
Kim Ho-Youn
Youn Jee-Hee
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Abstract
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K/BxN serum can transfer arthritis to normal mice owing to the abundant autoantibodies it contains, which trigger innate inflammatory cascades in joints. Little is known about wheth-er gut-residing microbes affect host susceptibility to auto-antibody-mediated arthritis. To address this, we fed C57BL/6 mice with water containing a mixture of antibiotics (ampi-cillin, vancomycin, neomycin, and metronidazol) for 2 weeks and then injected them with K/BxN serum. Antibiotic treat-ment significantly reduced the amount of bacterial genomic DNA isolated from fecal samples, in particular a gene encod-ing 16S ribosomal RNA derived from segmented filamentous bacteria. Arthritic signs, as indicated by the arthritic index and ankle thickness, were significantly attenuated in anti-biotic-treated mice compared with untreated controls. Peyer’s patches and mesenteric lymph nodes from anti-biotic-treated mice contained fewer IL-17-expressing cells than those from untreated mice. Antibiotic treatment re-duced serum C3 deposition in vitro via the alternative com-plement pathway. IL-17?/? congenic C57BL/6 mice were less susceptible to K/BxN serum-transferred arthritis than their wild-type littermates, but were still responsive to treat-ment with antibiotics. These results suggest that gut-resid-ing microbes, including segmented filamentous bacteria, in-duce IL-17 production in GALT and complement activation via the alternative complement pathway, which cause the host to be more susceptible to autoantibody-mediated arthritis.
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KEYWORD
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K/BxN serum-transferred arthritis, Gut-residing microbes, Antibiotics, IL-17, Segmented filamentous bacteria
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