IL-36G drives sepsis-induced lung injury via NF-κB-dependent activation of the NLRP3 inflammasome in macrophage pyroptosis

Key Points

• Investigate the role of IL-36G in sepsis-induced lung injury through the activation of the NLRP3 inflammasome and subsequent pyroptosis.
• Utilized in vivo models of sepsis to assess lung injury effects of IL-36G.
• Applied knockdown techniques to reduce IL-36G expression.
• Evaluated inflammation and tissue damage in response to IL-36G modulation.
• IL-36G activation correlated with increased pyroptosis and NLRP3 inflammasome activity.
• Knockdown of IL-36G significantly reduced inflammation and tissue damage in the lung.
• Findings suggest targeting IL-36G could have therapeutic benefits in sepsis-related lung injury.