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Immune and inflammatory responses play significant roles in paraquat (PQ)-induced acute lung injury (ALI), but the specific mechanisms remain unclear. Our study aimed to investigate the action of STING-IRF3 signaling on PQ-induced ALI in mice. Following PQ administration, samples were collected at 2, 12, 24, and 48 h for  in vivo  studies, and 24 h for  in vitro  studies. Following PQ administration (30 mg/kg, i.p.), injury to mouse lungs was evaluated by H&amp;E staining and wet/dry ratios, and lung oxidative damage was evaluated by MDA and SOD assays. The mRNA levels of  Sting ,  Irf3 , and  Ifnβ  were detected by RT-PCR, the expression of STING and IRF3 were assessed by western blotting and IHC/IF, and the secretion of IFNβ was detected by ELISA.  In vivo , PQ administration induced pathological changes and increased wet/dry ratios in lungs after 48 h.  Sting ,  Irf3 , and  Ifnβ  mRNA levels in lung tissues, STING and pIRF3 protein levels in lung tissues, and IFNβ secretion in serum, were upregulated by PQ in a time-dependent manner. PQ administration promoted IRF3 nuclear translocation in lung tissues after 48 h. The above changes were all attenuated by dexamethasone treatment (5 mg/kg, i.p., qd).  In vitro , PQ induced STING and IRF3 translocation.  Irf3  or  Sting  silencing decreased the mRNA levels and supernatant secretion of IFNβ in PQ-treated RAW264.7 mouse macrophages.  Sting  silencing also inhibited the protein and mRNA levels of IRF3  in vitro . Our study suggests that STING-IRF3 signaling contributes to PQ-induced ALI, providing new information for future treatment strategies.

The STING-IRF3 pathway contributes to paraquat-induced acute lung injury