In patients with pH1N1 pneumonia, there was sustained hyperactivation of the innate, proinflammatory cytokines (e.g. IL-6, CXCL8/IL-8, CCL2/MCP-1, sTNFR-1), which correlated with disease severity and outcomes; and in comparison with seasonal influenza, the adaptive Th1/Th17-immunity related cytokines (e.g. CXCL10/IP-10, CXCL9/MIG, IL-17A) were markedly suppressed. This evidence concerns the gene CCL2 and pneumonia.