The major findings can be summarized as follows: (1) PM2.5 induces airway inflammation and triggers pyroptotic cell death in bronchial epithelial cells; (2) MUC1 mitigates PM2.5-induced airway inflammation in vivo; (3) MUC1 suppresses PM2.5-induced inflammatory responses in 16HBE cells by inhibiting IRAK4 phosphorylation and downstream activation of the TLR4/IRAK4/NF-κB signaling pathway; (4) MUC1 attenuates PM2.5-induced pyroptosis through suppression of the TLR4/IRAK4/NF-κB axis and downstream activation of the NLRP3/GSDMD pathway. Here, NFKB1 is linked to inflammatory response.