A retrospective cohort study of 74 2009 H1N1 patients found that higher levels of proinflammatory cytokines and chemokines in plasma were observed in the ARDS-death group compared with the survived-without-ARDS or the mild-disease groups [5] . Another study in critically ill patients with ARDS caused by 2009 H1N1 virus infection has shown that the hallmarks of disease severity were elevated levels of IL-6, IL-15, IL-8 and TNF-a [36] . We examined the levels of five cytokines and chemokines in infected mouse lungs and found significant differences between the virus-infected and mock groups. It has proved that high levels of IL-6 were able to mediate acute lung injury [37] , and had a negative correlation with the Pa O2 :Fi O2 ratio in severely affected patients with 2009 H1N1 virus infection [36] . Our data showed SD/09 viral infection induced high levels of IL-6 in mouse lung, which may also play an important role in the course of ARDS. Hagau etc. found the levels of TNF-a increased significantly in the 2009 H1N1-related ARDS patients [36] . In present study, TNF levels also dramatically increased in the lungs of virus-infected mice, and were consistent with the clinical symptoms and reached peak levels when mice began to die. In addition, high levels of IL-10, IFN-c and MCP-1 were also present in the virus-infected mouse lungs, similar to observations found in severely affected humans with 2009 H1N1 infection [38] .