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Research Paper

Dysbiosis of gut microbiota induced the disorder of helper T cells in influenza virus-infected mice

, , , , , , , & show all
Pages 1140-1146 | Received 30 Oct 2014, Accepted 19 Dec 2014, Published online: 27 May 2015
 

Abstract

It is widely understood that commensal microbiota contributes to the maintenance of intestinal homeostasis through dynamic interactions with a body's immunity. And the immune regulation is important for the influenza vaccine's effectiveness after body injection, however, the mechanism between commensal microbiota and vaccine's effectiveness remains unknown. The impact that individual bacteria species have on the balance of the systemic immune system beyond the local intestinal mucosal tissues also remains less clear, and the related mechanism is still unknown. In this study, through the administration of various antibiotics, we examined the balance of helper T cell subsets in mice after inoculating them with the influenza virus and then, attempted to imitate the clinical practice in which patients are always prescribed with an antibiotic treatment in flu season. The data indicates that the mice in each group present differential immune responses in terms of the makeup of helper T cell subsets, although the Th17 cell activity seems to not be involved in the systemic immune modulation in the mice that are susceptible to the intervention of antibiotic. Th1, Th2, and anti-inflammatory regulatory T cells have been implicated in the contribution to the systemic immune response influenced by the antibiotic-induced dysbiosis. Thus we believe that the normal intestinal flora could maintain the immune balance and inhibit the inflammatory responses, which may be useful for clinical application to take intestinal flora into consideration when influenza vaccination was used.

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Funding

This work was funded by the National Natural Science Foundation of China (81473557 and 81273616), the Natural Science Foundation of Guangdong Province (S2013010013434), the Natural Science Foundation of Shandong Province (ZR2014HQ051) and the Science and Technology Program of Guangzhou (2014J4100106).

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