Late Breaking Abstract - Aggravated pathology in MRSA pneumonia secondary to Influenza A virus infection diverged from decreased expression of IL-1ß

Abstract

Background and Aims: Secondary methicillin resistant staphylococcus aureus (MRSA) infection enhances severity of viral pneumonia with high mortality during influenza A virus (IAV) pandemics. There were abundant researches found that NLRP3 inflammasome in macrophages played an important role in mediating inflammation and immunity by means of IL-1β both in IAV and MRSA infection respectively. However, the detailed activity and effect of NLRP3 inflammasome in aggravated pathology of lung in MRSA pneumonia secondary to IAV infection remain under debate. Methods: MRSA infection secondary to IAV was carried out both in vitro and in vivo in this research. Groups were set as blank group, IAV 1w group, and IAV 1w + MRSA 24h group both in murine macrophages and in mice. Then the expression of NLRP3, caspase-1, cleaved caspase-1, IL-1β and pathological change in lung were investigated by means of RT-qPCR, immunofluorescence, Western blot, ELISA and pathology. Results: The results firstly indicated that IAV infection for one week activated NLRP3 inflammasome, and MRSA infection secondary to IAV enhanced the expression of NLRP3, caspase-1 and cleaved caspase-1, but depressed the expression of IL-1β in vitro. The pneumonia model of mice was established successfully. The data of research in mice confirmed the findings in vitro. And worse condition of mice underwent secondary MRSA infection was in accordance with more severe inflammatory pathology in lung. Conclusion: Aggravated inflammatory pathology in MRSA pneumonia secondary to IAV infection diverged from decreased expression of IL-1β, which implied that excessive inflammatory pathology of lung was independent of IL-1β.