From triggers to asthma: a narrative review on epithelium dysfunction

Show more: Authors information and Publication history
Authors Information

1SOS Allergy and Clinical Immunology, USL Toscana Centro, Prato, Italy
2Centre of Bioclimatology, University of Florence, Florence, Italy
3Former Head of Pneumology and Chief of Department of Medicine and Rehabilitation, Guido Salvini Hospital-ASSTRhodense,Garbagnate Milanese, Milan, Italy
4UOC Pneumology, ASST-Rhodense, Garbagnate Milanese, Milan, Italy
5DISCLIMO - Department of Clinical and Molecular Sciences, Università Politecnica delle Marche, Italy
6Allergy Unit, Ospedali Riuniti Marche Nord, Fano, Italy
7Allergy Unit, National Healthcare System, Scilla, Italy
8Allergy Unit, Department of Internal Medicine, University Hospital Ospedali Riuniti di Ancona, Ancona, Italy  


Published: 10 October 2022
Accepted: 07 October 2022
Received: 06 October 2022


It is currently recognized that the airway epithelium plays a pivotal role in orchestrating inflammatory, immune, and regenerative responses to allergens, viruses and environmental pollutants that contribute to asthma pathogenesis. The impact of pollen on respiratory epithelium is multifaceted and goes beyond the direct barrier damage driven by the best-known Type-2 response. After pollen-driven activation, airway epithelial cells play an active role in triggering several pathways. In particular, the release of epithelial cytokines (or alarmins) activates both innate and adaptive immunity, with downstream effects implicated to the pathogenesis of asthma. Pollutants also have a pleiotropic effect on respiratory epithelium. Diesel exhaust particles can directly damage the respiratory epithelium with consequent barrier dysfunction, increased permeability, and local inflammation, but they can also activate Th2 responses. Innate immune responses also are triggered by pollutants through release of epithelial cytokines and redox-sensitive pathways that generate mechanical and immunologic changes in the respiratory epithelium. In addition to the typical Type-1 immune response, respiratory virus infections stimulate type-2 innate lymphoid cells in the airway epithelium to release epithelial cytokines. Finally, the action of epithelial triggers on airway smooth muscle is the central element in the induction of remodeling and hyperreactivity of the airways in asthma. This article reviews the pathophysiology and functions of the airway epithelium and the role of epithelial damage by different triggers in the development, persistence, and exacerbations of asthma.

Epithelial cytokines; airway epithelium;environment; barrier; allergy.

Table of Content: Vol. 54 (No. 6) 2022 November

European Annals of Allergy and Clinical Immunology ISSN 1764-1489 | © 2024