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The attenuation of Th1 and Th17 responses via autophagy protects against methicillin-resistant staphylococcus aureus-induced sepsis

Shufang Zhang  Xiaofang Huang  Huiqing Xiu  Zhongheng Zhang  Kai Zhang  Jiachang Cai  Zhijian Cai  Zhanghui Chen  Zhaocai Zhang  Wei Cui  Gensheng Zhang  Meixiang Xiang  
【摘要】:Background:Whether autophagy affects methicillin-resistant Staphylococcus aureus(MRSA)-induced sepsis and associated mechanisms are largely unknown.The purpose of the study was to investigate the role of autophagy and the contribution of autophagy to T helper(Th) 1 and Th17 responses in MRSA-induced sepsis.Methods:MRSA-induced sepsis was established by intravenous injection of USA300.Levels of microtubuleassociated protein 1 light chain 3(LC3)-II/I,Beclin-1 and p62 after USA300 infection were examined by western blot and immunohistochemical staining.Bacterial burden,hematoxylin-eosin staining,and Kaplan-Meier analysis were performed to evaluate the effect of autophagy on MRSA-induced sepsis.Interferon-γ(IFN-γ) and interleukin-17(IL-17) were analyzed by enzyme-linked immunosorbent assay,and CD4+ T cells differentiation was assessed by flow cytometry to observe the contribution of autophagy on Th1 and Th17 polarization after USA300 infection.Results:LC3-II/I and Beclin-1 were increased,while p62 were decreased after infection.Survival rates were decreased in LC3 B-/-and Beclin-1+/-groups(67% vs.25%;67% vs.33%,both P0.01),accompanied with aggravated organ injuries and increased IFN-γ and IL-17 in the serum;whereas rapamycin alleviated organ damages,decreased IFN-γ and IL-17,and improved survival rate(67% vs.92%,P0.01).However,there was no significant difference in bacterial burden.Flow cytometric analysis showed rapamycin treatment decreased the frequencies of Th1 and Th17 in the lymphocytes of spleen;whereas they were up-regulated in LC3 B-/-and Beclin-1+/-groups.Conclusions:Autophagy plays a protective role in MRSA-induced sepsis,which may be partly associated with the alleviation of organ injuries via the down-regulation of Th1 and Th17 response.

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