Gut-residing Microbes Alter the Host Susceptibility to Autoantibody-mediated Arthritisopen access
- Authors
- Lee, Hyerim; Jin, Bo-Eun; Jang, Eunkyeong; Lee, A Reum; Han, Dong Soo; Kim, Ho-Youn; Youn, Jee hee
- Issue Date
- Feb-2014
- Publisher
- 대한면역학회
- Keywords
- K/BxN serum-transferred arthritis; Gut-residing microbes; Antibiotics; IL-17; Segmented filamentous bacteria
- Citation
- Immune Network, v.14, no.1, pp.38 - 44
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- Immune Network
- Volume
- 14
- Number
- 1
- Start Page
- 38
- End Page
- 44
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/160682
- DOI
- 10.4110/in.2014.14.1.38
- ISSN
- 1598-2629
- Abstract
- 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 whether gut-residing microbes affect host susceptibility to autoantibody-mediated arthritis. To address this, we fed C57BL/6 mice with water containing a mixture of antibiotics (ampicillin, vancomycin, neomycin, and metronidazol) for 2 weeks and then injected them with K/BxN serum. Antibiotic treatment significantly reduced the amount of bacterial genomic DNA isolated from fecal samples, in particular a gene encoding 16S ribosomal RNA derived from segmented filamentous bacteria. Arthritic signs, as indicated by the arthritic index and ankle thickness, were significantly attenuated in antibiotic-treated mice compared with untreated controls. Peyer’s patches and mesenteric lymph nodes from antibiotic-treated mice contained fewer IL-17-expressing cells than those from untreated mice. Antibiotic treatment reduced serum C3 deposition in vitro via the alternative complement 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 treatment with antibiotics. These results suggest that gut-residing microbes, including segmented filamentous bacteria, induce 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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