Proteome profiling of the lung tissues of the mice co-infected with H9N2 influenza A virus and Pseudomonas aeruginosa.

H9N2 Influenza A virus (IAV) can contribute to Pseudomonas aeruginosa (P. aeruginosa) superinfection, causing severe pneumonia. But the underlying mechanisms remain unclear. In this study, to investigate molecular ecology of the lung tissues co-infected with H9N2 IAV and P. aeruginosa, the mouse models were developed to analyze proteome of the lung tissues. As a result, the differential proteins of the lungs sampled from the mice with single H9N2 IAV infection, single P. aeruginosa infection and co-infection with H9N2 IAV and P. aeruginosa were related to immune responses, cell proliferation and apoptosis, which were involved in NF-κB pathway, Toll-like signaling pathway, RIG-I signaling pathway and JAK-STAT signaling pathway. It implied that the different infection combinations of H9N2 IAV and P. aeruginosa influenced the protein expression levels. Based on the proteomics assays, the three proteins, NLRX1, ISG15 and IRF9, were screened to be further characterized using the in vitro MH-S cell models with H9N2 IAV and P. aeruginosa co-infection. The findings demonstrated that NLRX1, IRF9 and ISG15 might play the important roles in immune response against H9N2 IAV and P. aeruginosa co-infection and are potential targets for the development of drugs to prevent and treat the diseases.