Abstract
Background and Aims: Influenza A virus (IAV) is the major cause of severe viral pneumonia. The NLRP3 inflammasome in macrophages has been found essential for responsing against IAV infection. The pathology and immunity in IAV infection are self-limited to within one week commonly. Meanwhile, researches found that inflammation induced by NLRP3 inflammasome in the early and later stage of IAV infection was under debate. This study aims to investigate the detailed activity and role of NLRP3 inflammasome during IAV infection in vitro. Methods: After mouse macrophages were cultured and infected with IAV H1N1 for 6 hours (6h group) and one week (1w group) respectively, RT-qPCR was applied to detect the transcription of NLRP3, caspase-1 and IL-1β, western blot was used to detect the protein of NLRP3, caspase-1 and cleaved caspase-1, protein of NLRP3 in cells was also observed by immunofluorescent staining, and the concentration of IL-1β in supernatant was measured by ELISA. Results: In 6h group, the expression of NLRP3, caspase-1, cleaved caspase-1, IL-1β were increased compared with those of blank group (all P Conclusion: These findings confirmed that IAV infection activated NLRP3 inflammasome, and the divergent expression of NLRP3 from caspase-1 and IL-1β in 1w group suggested that the transcription and secretion of IL-1β was independent of NLRP3 in the later stage of IAV infection.
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