Gut-residing Microbes Alter the Host Susceptibility to Autoantibody-mediated Arthritis
DC Field | Value | Language |
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dc.contributor.author | Lee, Hyerim | - |
dc.contributor.author | Jin, Bo-Eun | - |
dc.contributor.author | Jang, Eunkyeong | - |
dc.contributor.author | Lee, A Reum | - |
dc.contributor.author | Han, Dong Soo | - |
dc.contributor.author | Kim, Ho-Youn | - |
dc.contributor.author | Youn, Jee hee | - |
dc.date.accessioned | 2022-07-16T06:05:50Z | - |
dc.date.available | 2022-07-16T06:05:50Z | - |
dc.date.created | 2021-05-13 | - |
dc.date.issued | 2014-02 | - |
dc.identifier.issn | 1598-2629 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/160682 | - |
dc.description.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. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | 대한면역학회 | - |
dc.title | Gut-residing Microbes Alter the Host Susceptibility to Autoantibody-mediated Arthritis | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Han, Dong Soo | - |
dc.contributor.affiliatedAuthor | Youn, Jee hee | - |
dc.identifier.doi | 10.4110/in.2014.14.1.38 | - |
dc.identifier.bibliographicCitation | Immune Network, v.14, no.1, pp.38 - 44 | - |
dc.relation.isPartOf | Immune Network | - |
dc.citation.title | Immune Network | - |
dc.citation.volume | 14 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 38 | - |
dc.citation.endPage | 44 | - |
dc.type.rims | ART | - |
dc.identifier.kciid | ART001916849 | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | Y | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.subject.keywordAuthor | K/BxN serum-transferred arthritis | - |
dc.subject.keywordAuthor | Gut-residing microbes | - |
dc.subject.keywordAuthor | Antibiotics | - |
dc.subject.keywordAuthor | IL-17 | - |
dc.subject.keywordAuthor | Segmented filamentous bacteria | - |
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