Stimulation of lipopolysaccharide from Pseudomonas aeruginosa following H9N2 IAV infection exacerbates inflammatory responses of alveolar macrophages and decreases virus replication

H9N2 IAV infection contributed to P. aeruginosa coinfection, causing severe hemorrhagic pneumonia in mink. In this study, the in vitro alveolar macrophage models were developed to investigate the innate immune responses to P. aeruginosa LPS stimulation following H9N2 IAV infection, using MH-S cells. The cytokine levels, apoptosis levels and the viral nucleic acid levels were detected and analyzed. As a result, the levels of IFN-& alpha;, IL-1 & beta;, TNF-& alpha;, and IL-10 in MH-S cells with P. aeruginosa LPS stimulation following H9N2 IAV infection were significantly higher than those in MH-S cells with single H9N2 IAV infection and single LPS stimulation (P < 0.05), exac-erbating inflammatory responses. LPS stimulation aggravated the apoptosis of MH-S cells with H9N2 IAV infection. Interestingly, LPS stimulation influences H9N2 IAV replication and indirectly reduced H9N2 IAV replications in in vitro AMs. It implied that LPS should play an important role in the pathogenesis of H9N2 IAV and P. aeruginosa coinfection.

Automated summary

H9N2 IAV infection contributes to severe hemorrhagic pneumonia and coinfection with P. aeruginosa in mink. This study investigates the innate immune responses to P. aeruginosa LPS stimulation following H9N2 IAV infection using an in vitro alveolar macrophage model. The results show that LPS stimulation exacerbates inflammatory responses and apoptosis in MH-S cells with H9N2 IAV infection, and also influences H9N2 IAV replication.