Subacute exposure of PM2.5 induces airway inflammation through inflammatory cell infiltration and cytokine expression in rats

Abstract

Accumulating evidences support that exposure to fine particulate matter (PM2.5) could cause inflammation of the airway, but its underlying mechanisms are less known. Our study aimed to explore the potential effect of non-canonical NF-κB signaling pathway in airway inflammation, which caused by PM2.5, and the possible regulatory relationship between miR-6747–5p and NF-κB2. The histological analysis from in vivo study manifested that PM2.5 could induce the exudation and infiltration of polymorphonuclear leukocytes (PMNs). Immunohistochemistry results of lung tissues showed that PM2.5 increased ICAM-1, 6Ckine, SDF-1 and BAFF positive staining with a dose-dependent manner. In addition, PM2.5 could induce the p52 nuclear translocation to trigger non-canonical NF-κB signaling pathway in lung tissues and BEAS-2B cells. Targetscan reporter gene assay showed that there was a target regulatory relationship between miR-6747–5p and NF-κB2. Besides, the chemical mimics of miR-6747–5p weakened the activation of non-canonical NF-κB signaling pathway induced by PM2.5. In summary, exposure to PM2.5 could trigger airway inflammation by activating the non-canonical NF-κB signaling pathway, which may be related to the negative feedback regulation mechanism of miR-6747–5p. Our findings will give new ideas into the toxic effects of airway inflammation triggered by PM2.5.