Collectively, H9N2 AIV infection enhanced the expression of proinflammatory cytokines, such as IFN-α, IL-17A, IFN-γ, and IL-22, and promoted the proliferation and translocation of Proteobacteria, especially E. coli, which might be induced by the injury of mucous layers and tight junctions. The gene discussed is IFNG; the disease is infection.