Clindamycin Administration Increases the Incidence of Collagen-Induced Arthritis in Mice Through the Prolonged Impact of
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ORIGINAL ARTICLE
Clindamycin Administration Increases the Incidence of Collagen-Induced Arthritis in Mice Through the Prolonged Impact of Gut Immunity Shukai Yang,1 Huijuan Chen,2 Bo Wei,1 Min Xiang,1 Zibing Hu,1 Zhiheng Peng,1 Hao Lin,1 and Jiecong Sun 1,3
Abstract—The profound influence of gut flora on host immune system and its link with autoi-
mmune disorders have been established. However, the role of certain antibiotic in progression of autoimmune disorder is still confusing. Here, we employed a collagen-induced arthritis (CIA) model to explore the role of clindamycin administration in different scenarios. In the first scenario, mice treated with antibiotics for 4 weeks were performed with the induction of CIA immediately. The results showed that clindamycin administration promoted the incidence and severity of CIA, while the recipients of vancomycin showed completed tolerance. We also found that increased gut-associated Th1 and Th17 cells might be related to the subsequent expansion of collagen-specific immune response. In the second scenario, mice treated with antibiotics for 4 weeks were performed with CIA induction 4 weeks later. Notably, clindamycin administration showed a prolonged impact on the incidence and severity of CIA, as well as the gut immunity as compared to vancomycin administration. In addition, antibody depletion of integrin α4β7 systemically resulted in an impaired CIA response, underlining the influence of gut immunity. In the mice that received clindamycin, the abundance of anaerobic bacteria was significantly decreased and showed little recovery at 4 weeks later. Our observations highlighted the different characteristics of antibiotic administration on the development of autoimmune disorders and indicated its link with gut immunity. KEY WORDS: antibiotics; gut flora; immunity; collagen-induced arthritis.
INTRODUCTION Rheumatoid arthritis (RA) is an autoimmune disorder characterized by CD4+ and neutrophil infiltration, leading to chronic joint and synovial destruction [1–3]. The 1
Department of Orthopedics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524001, People’s Republic of China 2 Gynaecology and Obstetrics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524001, People’s Republic of China 3 To whom correspondence should be addressed at Department of Orthopedics, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524001, People’s Republic of China. E-mail: [email protected]
etiopathogenesis of RA is still confusing, but rising evidences indicate that both genetic factors and environmental factors, including microbes and infection, are involved [4]. The relationship of RA and several individual microorganisms have been clearly established [5]. For instances, the amount of Lactobacillus salivarius in digestive tract is associated with the severity of RA in patients [6]. Introduction of a single bacteria segmented filamentous bacteria increases the morbidity of arthritis in experimental mice [7].
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