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Review
. 2025 Jun;18(3):524-536.
doi: 10.1016/j.mucimm.2025.03.003. Epub 2025 Mar 26.

Airway epithelial cells as drivers of severe asthma pathogenesis

Del Dorscheid  1 , Gail M Gauvreau  2 , Steve N Georas  3 , Pieter S Hiemstra  4 , Gilda Varricchi  5 , Bart N Lambrecht  6 , Gianni Marone  7
Affiliations
Free article
Review

Airway epithelial cells as drivers of severe asthma pathogenesis

Del Dorscheid et al. Mucosal Immunol. 2025 Jun.
Free article

Abstract

Our understanding of the airway epithelium's role in driving asthma pathogenesis has evolved over time. From being regarded primarily as a physical barrier that could be damaged via inflammation, the epithelium is now known to actively contribute to asthma development through interactions with the immune system. The airway epithelium contains multiple cell types with specialized functions spanning barrier action, mucociliary clearance, immune cell recruitment, and maintenance of tissue homeostasis. Environmental insults may cause direct or indirect injury to the epithelium leading to impaired barrier function, epithelial remodelling, and increased release of inflammatory mediators. In severe asthma, the epithelial barrier repair process is inhibited and the response to insults is exaggerated, driving downstream inflammation. Genetic and epigenetic mechanisms also maintain dysregulation of the epithelial barrier, adding to disease chronicity. Here, we review the role of the airway epithelium in severe asthma and how targeting the epithelium can contribute to asthma treatment.

Keywords: Airway epithelium; Asthma pathogenesis; Immune system; Severe asthma.

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Conflict of interest statement

Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: D.D. is supported by the following grants and clinical trials: AstraZeneca, British Columbia Lung Association, Canadian Institutes of Health Research, Michael Smith Foundation for Health Research, Teva Pharmaceuticals, and Sanofi Regeneron; he has also received speaking fees, travel grants, unrestricted project grants, and writing fees, and is a paid consultant via ad boards and other mechanisms for AstraZeneca, GSK, Novartis Canada, Sanofi Regeneron, and Valeo Pharma. G.M.G. reports personal fees from AstraZeneca, Novartis, Sterna Biologicals, and Third Harmonic Bio, and reports research grants from AstraZeneca, BioGaia, Biohaven, Genentech, and Novartis. S.N.G. has received consulting fees from AstraZeneca, ARS Pharma, Chiesi, Inc., and Merck. P.S.H. has received service fees from AstraZeneca. G.V. has received grants from AstraZeneca. B.N.L. is supported by grants from the European Research Council, Ghent University, Research Foundation Flanders (FWO), and Flanders Institute of Biotechnology (VIB), and has received consulting fees from Argenx, AstraZeneca, GSK, and Sanofi. G.M. is supported by grants from the University of Naples Federico II, Naples Italy and the National Research Council, Italy, and has received consulting fees from AstraZeneca.