Enhanced activity of NLRP3 inflammasome and its proinflammatory effect in influenza A viral pneumonia

Aim: The aim of this study was to investigate the activity of NLRP3 inflammasome and its effect on inducing severe pneumonia 1 week after influenza A virus (IAV) infection. Materials & methods: The expression levels of NLRP3, caspase-1 and IL-1 beta were assessed in murine macrophages stimulated with IAV. And the severity of viral pneumonia in mice was explored. Results & conclusion: The data showed that although the expression of NLRP3 diverged, activity of NLRP3 inflammasome was enhanced 1 week after IAV infection, and more severe viral pneumonia was associated with IL-1 beta in serum. It infers that enhanced activity of NLRP3 inflammasome induces augmented expression of IL-1 beta and severe pneumonia in a NLRP3-independent way, 1 week after IAV infection. Plain language summary: Influenza A virus (IAV) infects lungs. Inflammasome is a complex of proteins in cells. It plays key role in IAV infection. We studied the role of NLRP3 inflammasome. The results are shown as below. The expression of IL-1 beta increased. Severer pneumonia was related with it. However, the expression of NLRP3 decreased. It diverged from that of IL-1 beta. Three conclusions were drawn. IAV infection activates NLRP3 inflammasome. Upregulation of IL-1 beta 1 week after infection induces severe pneumonia. It is independent of NLRP3. Tweetable abstract: Data from biomedical research suggests that divergent activity and role of NLRP3 inflammasome during influenza A virus infection should be considered.