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Russo, R.C.* ; Togbe, D.* ; Couillin, I.* ; Segueni, N.* ; Han, L. ; Quesniaux, V.F.J.* ; Stöger, T. ; Ryffel, B.*

Ozone-induced lung injury and inflammation: Pathways and therapeutic targets for pulmonary diseases caused by air pollutants.

Environ. Int. 198:109391 (2025)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Exposure to ambient Ozone (O3) air pollution directly causes by its oxidative properties, respiratory epithelial cell injury, and cell death, which promote inflammation and hyperreactivity, posing a significant public health concern. Recent clinical and experimental studies have made strides in elucidating the mechanisms underlying O3-induced epithelial cell injury, inflammation, and airway hyperreactivity, which are discussed herein. The current data suggest that O3-induced oxidative stress is a central event-inducing oxeiptotic cell death pathway. O3-induced epithelial barrier damage and cell death, triggering the release of alarmins and damage-associated molecular patterns (DAMPs), with subsequent endogenous activation of Toll-like receptors (TLRs), DNA sensing pathways, and inflammasomes, activating interleukin-1-Myd88 inflammatory pathway with the production of a range of chemokines and cytokines. This cascade orchestrates lung tissue-resident cell activation in response to O3 in leukocyte and non-leukocyte populations, driving sterile innate immune response. Chronic inflammatory response to O3, by repeated exposures, supports a mixed phenotype combining asthma and emphysema, in which their exacerbation by other particulate pollutants potentially culminates in respiratory failure. We use data from lung single-cell transcriptomics to map genes of O3-damage sensing and signaling pathways to lung cells and thereby highlight potential hotspots of O3 responses. Deeper insights into these pathological pathways might be helpful for the identification of novel therapeutic targets and strategies.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Schlagwörter Alarmins ; Damps ; Il-33 ; Inflammasome ; O(3) ; Pollution; Growth-factor-beta; Toll-like Receptors; Nlrp3 Inflammasome; Nalp3 Inflammasome; Oxidative Stress; Innate Immunity; Mouse Model; Induced Neutrophil; Epithelial-cells; Subacute Ozone
Sprache englisch
Veröffentlichungsjahr 2025
HGF-Berichtsjahr 2025
ISSN (print) / ISBN 0160-4120
e-ISSN 1873-6750
Zeitschrift Environment International
Quellenangaben Band: 198, Heft: , Seiten: , Artikelnummer: 109391 Supplement: ,
Verlag Elsevier
Verlagsort The Boulevard, Langford Lane, Kidlington, Oxford Ox5 1gb, England
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Lung Health and Immunity (LHI)
POF Topic(s) 30202 - Environmental Health
Forschungsfeld(er) Lung Research
PSP-Element(e) G-505000-001
Förderungen Artimmune SAS
University of Orleans
Fondation pour la Recherche Medicale' (FRM)
European Union
Region Centre-Val de Loire
Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq - Brazil)
Fundacao de Amparo a Pesquisa de Minas Gerais (FAPEMIG - Brazil)
Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
Le Studium Visiting Researcher 2023 of the Smart Loire Valley
Centre National de la Recherche Scientifique (CNRS)
DOI 10.1016/j.envint.2025.109391
WOS ID 001455601300001
Scopus ID 105000691652
PubMed ID 40121788
Erfassungsdatum 2025-05-09
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