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PM2.5 induced pulmonary fibrosis in vivo and in vitro

Zihan Xu1, Zilin Li1, Ziyi Liao1

  • 1Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.

Ecotoxicology and Environmental Safety
|January 1, 2019
PubMed

Insights

Particulate matter (PM2.5) exposure causes lung inflammation and fibrosis by activating the TGF-β1/SMAD3 pathway in lung cells. This study reveals PM2.5 as a potent initiator of pulmonary fibrosis (PF) through epithelial, macrophage, and fibroblast targeting.

Area of Science:

  • Environmental Health
  • Pulmonary Medicine
  • Toxicology

Background:

  • Epidemiological studies link fine particulate matter (PM2.5) exposure to pulmonary fibrosis (PF).
  • The precise mechanisms by which PM2.5 induces PF remain incompletely understood.
  • Investigating PM2.5's role in PF pathogenesis is crucial for public health.

Purpose of the Study:

  • To elucidate the in vivo and in vitro mechanisms of PM2.5-induced pulmonary fibrosis.
  • To determine the cellular targets and signaling pathways involved in PM2.5-mediated lung injury.
  • To assess the expression of key fibrotic markers following PM2.5 exposure.

Main Methods:

  • Mice were exposed to PM2.5 intranasally for 4 weeks.
  • Lung tissue and serum were analyzed using Micro-CT, HE staining, and ELISA.
  • Human bronchial epithelial (BEAS-2B), pulmonary fibroblast (HFL-1), and macrophage (RAW264.7) cell lines were treated with PM2.5.
  • TGF-β1/SMAD3 pathway activation, epithelial-mesenchymal transition (EMT), and fibrotic marker expression were assessed.

Main Results:

  • PM2.5 exposure induced lung inflammation and fibrosis in mice, increasing TGF-β1, α-SMA, and COL1 expression.
  • In vitro, PM2.5 activated the TGF-β1/SMAD3 pathway, induced EMT in BEAS-2B cells, and promoted HFL-1 cell differentiation.
  • Conditioned media from PM2.5-treated BEAS-2B and RAW264.7 cells stimulated fibrotic responses in HFL-1 cells.

Conclusions:

  • PM2.5 exposure initiates pulmonary fibrosis by targeting pulmonary epithelium, macrophages, and fibroblasts.
  • The TGF-β1/SMAD3 signaling pathway plays a critical role in PM2.5-induced fibrotic responses.
  • PM2.5 is identified as a significant initiator of pulmonary fibrosis.
Keywords:
EMTPM(2.5)Pulmonary fibrosisTGF-β1

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