NLRP3 protein deficiency exacerbates hyperoxia-induced lethality through stat3 protein signaling independent of interleukin-1β

Abstract

Background: The role of NLRP3 inflammasomes in hyperoxic acute lung injury (HALI) remains unclear. Results: NLRP3 deficiency exacerbated lethality and diminished Stat3 activation caused by inflammatory cells in a murine HALI model. Conclusion: NLRP3 regulates Stat3 activation by affecting inflammatory cell infiltration independent of IL-1β. Significance: These findings demonstrate the novel role of NLRP3 in Stat3-mediated protective effects against HALI.