Oxidative stress-induced inflammation in susceptible airways by anthropogenic aerosol

Leni, Zaira; Cassagnes, Laure Estelle; Daellenbach, Kaspar R.; El Haddad, Imad; Vlachou, Athanasia; Uzu, Gaelle; Prévôt, André S. H.; Jaffrezo, Jean-Luc; Baumlin, Nathalie; Salathe, Matthias; Baltensperger, Urs; Dommen, Josef; Geiser, Marianne (2020). Oxidative stress-induced inflammation in susceptible airways by anthropogenic aerosol. PLoS ONE, 15(11), e0233425. Public Library of Science 10.1371/journal.pone.0233425

[img]
Preview
Text
journal.pone.0233425.pdf - Published Version
Available under License Creative Commons: Attribution (CC-BY).

Download (2MB) | Preview

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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy > Cell Biology

UniBE Contributor:

Leni, Zaira and Geiser, Marianne

Subjects:

600 Technology > 610 Medicine & health
500 Science > 570 Life sciences; biology

ISSN:

1932-6203

Publisher:

Public Library of Science

Funders:

[42] Schweizerischer Nationalfonds

Language:

English

Submitter:

Marianne Geiser Kamber

Date Deposited:

08 Dec 2020 09:41

Last Modified:

13 Dec 2020 02:51

Publisher DOI:

10.1371/journal.pone.0233425

PubMed ID:

33206642

BORIS DOI:

10.7892/boris.148595

URI:

https://boris.unibe.ch/id/eprint/148595

Actions (login required)

Edit item Edit item
Provide Feedback