Gut-residing Microbes Alter the Host Susceptibility to Autoantibody-mediated Arthritis
Immune Network
; : 38-44, 2014.
Article
en En
| WPRIM
| ID: wpr-192386
Biblioteca responsable:
WPRO
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.
Palabras clave
Texto completo:
1
Índice:
WPRIM
Asunto principal:
Ganglios Linfáticos Agregados
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Artritis
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Autoanticuerpos
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Bacterias
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ADN
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ARN Ribosómico 16S
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Agua
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Neomicina
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Vancomicina
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Genes vif
Límite:
Animals
Idioma:
En
Revista:
Immune Network
Año:
2014
Tipo del documento:
Article