Gut-residing Microbes Alter the Host Susceptibility to Autoantibody-mediated Arthritis.
- Author:
Hyerim LEE
1
;
Bo Eun JIN
;
Eunkyeong JANG
;
A Reum LEE
;
Dong Soo HAN
;
Ho Youn KIM
;
Jeehee YOUN
Author Information
- Publication Type:In Vitro ; Original Article
- Keywords: K/BxN serum-transferred arthritis; Gut-residing microbes; Antibiotics; IL-17; Segmented filamentous bacteria
- MeSH: Animals; Ankle; Anti-Bacterial Agents; Arthritis*; Autoantibodies; Bacteria; Complement Activation; Complement Pathway, Alternative; DNA; Genes, vif; Interleukin-17; Joints; Lymph Nodes; Mice; Neomycin; Peyer's Patches; RNA, Ribosomal, 16S; Vancomycin; Water
- From:Immune Network 2014;14(1):38-44
- CountryRepublic of Korea
- Language:English
- 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.
