PPAR-gamma regulates PFAS-mediated proinflammatory cytokines in lung epithelial cells.

ABSTRACT:

Background

Per and polyfluoroalkyl substances (PFAS), including the legacy compound perfluorooctanesulfonic acid (PFOS), are persistent organic pollutants with long biological half-lives. Emerging evidence suggests a significant accumulation of PFAS/PFOS in the human lung, potentially contributing to inflammation and altered immune responses. However, the role of peroxisome proliferator-activated receptor gamma (PPARγ) signaling in PFAS/PFOS-induced pulmonary toxicity remains unclear.

Methods

Primary human bronchial epithelial (NHBE) cells were exposed to 15 µM binary PFAS mixture (PFOS + PFOA) or quaternary mixture (PFOS, PFOA, PFHxS, GenX) with or without the PPARγ antagonist (15 µM) and/or the PPARγ agonists rosiglitazone (10 µM) or pioglitazone (10 µM) for 24 h. BALB/c m

SUBMITTER: Shaikh SB 

PROVIDER: S-EPMC12910160 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature