Oxidative stress-induced inflammation in susceptible airways by anthropogenic aerosol.
- Leni Z Institute of Anatomy, University of Bern, Bern, Switzerland.
- Cassagnes LE Laboratory of Atmospheric Chemistry, Paul Scherrer Institute, Villigen, Switzerland.
- Daellenbach KR Laboratory of Atmospheric Chemistry, Paul Scherrer Institute, Villigen, Switzerland.
- El Haddad I Laboratory of Atmospheric Chemistry, Paul Scherrer Institute, Villigen, Switzerland.
- Vlachou A Laboratory of Atmospheric Chemistry, Paul Scherrer Institute, Villigen, Switzerland.
- Uzu G Univ. Grenoble Alpes, CNRS, IRD, INP, IGE, Grenoble, France.
- Prévôt ASH Laboratory of Atmospheric Chemistry, Paul Scherrer Institute, Villigen, Switzerland.
- Jaffrezo JL Univ. Grenoble Alpes, CNRS, IRD, INP, IGE, Grenoble, France.
- Baumlin N Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS, United States of America.
- Salathe M Department of Internal Medicine, University of Kansas Medical Center, Kansas City, KS, United States of America.
- Baltensperger U Laboratory of Atmospheric Chemistry, Paul Scherrer Institute, Villigen, Switzerland.
- Dommen J Laboratory of Atmospheric Chemistry, Paul Scherrer Institute, Villigen, Switzerland.
- Geiser M Institute of Anatomy, University of Bern, Bern, Switzerland.
- 2020-11-18
Published in:
- PloS one. - 2020
General Biochemistry, Genetics and Molecular Biology
General Agricultural and Biological Sciences
General Medicine
English
Ambient air pollution is one of the leading five health risks worldwide. One of the most harmful air pollutants is particulate matter (PM), which has different physical characteristics (particle size and number, surface area and morphology) and a highly complex and variable chemical composition. Our goal was first to comparatively assess the effects of exposure to PM regarding cytotoxicity, release of pro-inflammatory mediators and gene expression in human bronchial epithelia (HBE) reflecting normal and compromised health status. Second, we aimed at evaluating the impact of various PM components from anthropogenic and biogenic sources on the cellular responses. Air-liquid interface (ALI) cultures of fully differentiated HBE derived from normal and cystic fibrosis (CF) donor lungs were exposed at the apical cell surface to water-soluble PM filter extracts for 4 h. The particle dose deposited on cells was 0.9-2.5 and 8.8-25.4 μg per cm2 of cell culture area for low and high PM doses, respectively. Both normal and CF HBE show a clear dose-response relationship with increasing cytotoxicity at higher PM concentrations. The concurrently enhanced release of pro-inflammatory mediators at higher PM exposure levels links cytotoxicity to inflammatory processes. Further, the PM exposure deregulates genes involved in oxidative stress and inflammatory pathways leading to an imbalance of the antioxidant system. Moreover, we identify compromised defense against PM in CF epithelia promoting exacerbation and aggravation of disease. We also demonstrate that the adverse health outcome induced by PM exposure in normal and particularly in susceptible bronchial epithelia is magnified by anthropogenic PM components. Thus, including health-relevant PM components in regulatory guidelines will result in substantial human health benefits and improve protection of the vulnerable population.
- Language
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- English
- Open access status
- gold
- Identifiers
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- DOI 10.1371/journal.pone.0233425
- PMID 33206642
- Persistent URL
- https://folia.unifr.ch/global/documents/142641
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