Clindamycin Administration Increases the Incidence of Collagen-Induced Arthritis in Mice Through the Prolonged Impact of Gut Immunity.

Abstract

The profound influence of gut flora on host immune system and its link with autoimmune 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 4weeks 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 4weeks were performed with CIA induction 4weeks 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 4weeks later. Our observations highlighted the different characteristics of antibiotic administration on the development of autoimmune disorders and indicated its link with gut immunity.