Imperial College London
Alternate

ProfessorFanChung

Faculty of Medicine, National Heart & Lung Institute

Professor of Respiratory Medicine
 
 
 
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Contact

 

+44 (0)20 7594 7954f.chung Website

 
 
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Assistant

 

Miss Carolyn Green +44 (0)20 7594 7959

 
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Location

 

227BGuy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Raby:2023:10.3389/fimmu.2023.1201658,
author = {Raby, KL and Michaeloudes, C and Tonkin, J and Chung, KF and Bhavsar, PK},
doi = {10.3389/fimmu.2023.1201658},
journal = {Frontiers in Immunology},
pages = {1--14},
title = {Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD},
url = {http://dx.doi.org/10.3389/fimmu.2023.1201658},
volume = {14},
year = {2023}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - The airway epithelium comprises of different cell types and acts as a physical barrier preventing pathogens, including inhaled particles and microbes, from entering the lungs. Goblet cells and submucosal glands produce mucus that traps pathogens, which are expelled from the respiratory tract by ciliated cells. Basal cells act as progenitor cells, differentiating into different epithelial cell types, to maintain homeostasis following injury. Adherens and tight junctions between cells maintain the epithelial barrier function and regulate the movement of molecules across it. In this review we discuss how abnormal epithelial structure and function, caused by chronic injury and abnormal repair, drives airway disease and specifically asthma and chronic obstructive pulmonary disease (COPD). In both diseases, inhaled allergens, pollutants and microbes disrupt junctional complexes and promote cell death, impairing the barrier function and leading to increased penetration of pathogens and a constant airway immune response. In asthma, the inflammatory response precipitates the epithelial injury and drives abnormal basal cell differentiation. This leads to reduced ciliated cells, goblet cell hyperplasia and increased epithelial mesenchymal transition, which contribute to impaired mucociliary clearance and airway remodelling. In COPD, chronic oxidative stress and inflammation trigger premature epithelial cell senescence, which contributes to loss of epithelial integrity and airway inflammation and remodelling. Increased numbers of basal cells showing deregulated differentiation, contributes to ciliary dysfunction and mucous hyperproduction in COPD airways. Defective antioxidant, antiviral and damage repair mechanisms, possibly due to genetic or epigenetic factors, may confer susceptibility to airway epithelial dysfunction in these diseases. The current evidence suggests that a constant cycle of injury and abnormal repair of the epithelium drives chronic airway inflammation and r
AU  - Raby,KL
AU  - Michaeloudes,C
AU  - Tonkin,J
AU  - Chung,KF
AU  - Bhavsar,PK
DO  - 10.3389/fimmu.2023.1201658
EP  - 14
PY  - 2023///
SN  - 1664-3224
SP  - 1
TI  - Mechanisms of airway epithelial injury and abnormal repair in asthma and COPD
T2  - Frontiers in Immunology
UR  - http://dx.doi.org/10.3389/fimmu.2023.1201658
UR  - https://www.ncbi.nlm.nih.gov/pubmed/37520564
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2023.1201658/full
UR  - http://hdl.handle.net/10044/1/105769
VL  - 14
ER  -
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