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Cellular response and extracellular vesicles characterization of human macrophages exposed to fine atmospheric

Perrine J Martin1, Amélie Héliot1, Gauthier Trémolet1

  • 1University of Littoral Côte d'Opale, Unit of Environmental Chemistry and Interactions with Life, UCEIV EA4492, SFR Condorcet FR CNRS 3417, Dunkerque, France.

Environmental Pollution (Barking, Essex : 1987)
|August 6, 2019
PubMed

Insights

Fine particulate matter (PM) exposure triggers inflammatory lung diseases. Infiltrating macrophages release extracellular vesicles (EVs) that promote inflammation in lung epithelial cells, suggesting EVs mediate PM-induced lung inflammation.

Area of Science:

  • Environmental Health
  • Pulmonary Toxicology
  • Cell Biology

Background:

  • Fine particulate matter (PM) is a major environmental cause of inflammatory lung diseases like COPD and asthma.
  • Alveolar macrophages are the first line of defense against PM, initiating inflammatory responses and recruiting other macrophages.

Purpose of the Study:

  • To investigate the gene expression, cytokine production, and extracellular vesicle (EV) release by infiltrating macrophages exposed to PM.
  • To assess the capacity of PM-induced EVs to transfer inflammatory signals to pulmonary epithelial cells.

Main Methods:

  • In vitro exposure of infiltrating macrophages to varying concentrations of fine PM.
  • Analysis of gene expression for Xenobiotic Metabolizing Enzymes (XMEs) and oxidative stress markers.
  • Quantification of cytokine production and EV release.
  • Co-culture experiments with pulmonary epithelial cells to evaluate EV-mediated effects.

Main Results:

  • PM exposure induced a dose-dependent increase in XME expression (e.g., CYP1A1, CYP1B1), oxidative stress enzymes (e.g., SOD2), and pro-inflammatory cytokines in macrophages.
  • PM exposure significantly increased EV release from macrophages in a dose-dependent manner.
  • EVs derived from PM-exposed macrophages induced a pro-inflammatory phenotype in pulmonary epithelial cells, marked by IL6 and TNFα release.

Conclusions:

  • Infiltrating macrophages contribute to PM-induced lung inflammation through both direct responses and EV-mediated signaling.
  • Extracellular vesicles play a role in propagating inflammatory signals from macrophages to lung epithelial cells following PM exposure.
Keywords:
Extracellular vesiclesFine atmospheric particulate matterInfiltrating macrophagesLung epithelial cells

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