MUC1 alleviates PM2.5-induced airway inflammation by inhibiting the IRAK4/NF-κB/NLRP3 mediated pyroptosis in airway epithelial cells.

ABSTRACT:

Backgrounds

Exposure to fine particulate matter (PM2.5) triggers airway inflammation through the activation of the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway, contributing to the pathogenesis of various acute and chronic respiratory diseases. Mucin 1 (MUC1), a transmembrane glycoprotein highly expressed on airway epithelial cells, is known to modulate TLR-mediated inflammatory responses. However, the specific role and molecular mechanism by which MUC1 regulates PM2.5-induced airway inflammation remain inadequately understood.

Methods

Lung injury models were established using Muc1^+/+ and Muc1^-/- rats via intranasal instillation of PM2.5. Histopathological changes and inflammatory responses were evaluated following treatment.

SUBMITTER: Zhou Y 

PROVIDER: S-EPMC12571608 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature