Kupffer cells contribute to concanavalin A-induced hepatic injury through a Th1 but not Th17 type response-dependent pathway in mice

查看全文 作　　者：Lin Chen,Xiao-Jun Xie,Yu-Fu Ye,Lin Zhou,Hai-Yang Xie,Qin-Fen Xie, Jiong Tian and Shu-Sen ZhengZhejiang University School of Medicine,Hangzhou 310003,ChinaKey Laboratory of Combined Multi-organ Transplantation,Ministry of Public Health;Department of Hepatobiliary and Pancreatic Surgery Department of Nephrology,First Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310003,China

出　　处：《Hepatobiliary & Pancreatic Diseases International》索引2011年第10卷第2期,共8页

基　　金：supported by grants from the National Basic Research Program of China(973 Program)(2009CB522403);the Key Program of the National Natural Science Foundation of China(30730085);the National Natural Science Youth Foundation of China(J20090846) 摘　　要：BACKGROUND:Increasing evidence suggests that a close interaction of Kupffer cells with T cells plays a central role in concanavalin A-induced hepatic injury in mice,but the underlying mechanisms remain obscure.The present study aimed to determine the relative roles of Th1 and Th17 type responses in concanavalin A-induced hepatic injury in mice, and to investigate whether or not Kupffer cells contribute to hepatic injury via a Th1 or Th17 type response-dependent pathway. METHODS:Immune-mediated hepatic injury was induced in C57BL/6 mice by intravenous injection of concanavalin A. Kupffer cells were inactivated by pretreatment with gadolinium chloride 24 hours before the concanavalin A injection.The interferon-gamma(IFN-γ)and interleukin-17(IL-17)pathways were blocked by specific neutralizing antibodies.Hepatic injury was assessed using serum transferase activity and pathological analysis.Expression of inflammatory cytokines within the liver was detected by real-time polymerase chain reaction and immunohistochemistry. RESULTS:Neutralization of IFN-γsignificantly attenuated concanavalin A-induced hepatic injury.However,neutralization of IL-17 failed to suppress the injury.Inactivation of Kupffer cells by gadolinium chloride pretreatment protected against concanavalin A-induced injury and significantly reduced hepatic cytokine levels including TNF-α,IL-6 and IFN-γbut not IL-17.CONCLUSION:Our findings suggest that Kupffer cells contribute to concanavalin A-induced hepatic injury via a Th1 type response-dependent pathway and production of inflammatory cytokines including TNF-α,IL-6 and IFN-γ. 关键词：KUPFFER cells INTERFERON-GAMMA INTERLEUKIN-17 concanavalin A hepatic injury HEPATITIS

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Kupffer cells contribute to concanavalin A-induced hepatic injury through a Th1 but not Th17 type response-dependent pathway in mice

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