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Epithelial function and dysfunction in asthma

Epithelial function and dysfunction in asthma
Epithelial function and dysfunction in asthma
Asthma was previously defined as an allergic Th2‐mediated inflammatory immune disorder. Recently, this paradigm has been challenged because not all pathological changes observed in the asthmatic airways are adequately explained simply as a result of Th2‐mediated processes. Contemporary thought holds that asthma is a complex immune disorder involving innate as well as adaptive immune responses, with the clinical heterogeneity of asthma perhaps a result of the different relative contribution of these two systems to the disease. Epidemiological studies show that exposure to certain environmental substances is strongly associated with the risk of developing asthma. The airway epithelium is first barrier to interact with, and respond to, environmental agents (pollution, viral infection, allergens), suggesting that it is a key player in the pathology of asthma. Epithelial cells play a key role in the regulation of tissue homeostasis by the modulation of numerous molecules, from antioxidants and lipid mediators to growth factors, cytokines, and chemokines. Additionally, the epithelium is also able to suppress mechanisms involved in, for example, inflammation in order to maintain homeostasis. An intrinsic alteration or defect in these regulation mechanisms compromises the epithelial barrier, and therefore, the barrier may be more prone to environmental substances and thus more likely to exhibit an asthmatic phenotype. In support of this, polymorphisms in a number of genes that are expressed in the bronchial epithelium have been linked to asthma susceptibility, while environmental factors may affect epigenetic mechanisms that can alter epithelial function and response to environmental insults. A detailed understanding of the regulatory role of the airway epithelium is required to develop new therapeutic strategies for asthma that not only address the symptoms but also the underlining pathogenic mechanism(s) and prevent airway remodelling.
0954-7894
Loxham, Matthew
8ef02171-9040-4c1d-8452-2ca34c56facb
Davies, Donna
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Blume, Cornelia
aa391c64-8718-4238-906b-d6bb1551a07b
Loxham, Matthew
8ef02171-9040-4c1d-8452-2ca34c56facb
Davies, Donna
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Blume, Cornelia
aa391c64-8718-4238-906b-d6bb1551a07b

Loxham, Matthew, Davies, Donna and Blume, Cornelia (2014) Epithelial function and dysfunction in asthma. Clinical & Experimental Allergy, 44 (11). (doi:10.1111/cea.12309).

Record type: Article

Abstract

Asthma was previously defined as an allergic Th2‐mediated inflammatory immune disorder. Recently, this paradigm has been challenged because not all pathological changes observed in the asthmatic airways are adequately explained simply as a result of Th2‐mediated processes. Contemporary thought holds that asthma is a complex immune disorder involving innate as well as adaptive immune responses, with the clinical heterogeneity of asthma perhaps a result of the different relative contribution of these two systems to the disease. Epidemiological studies show that exposure to certain environmental substances is strongly associated with the risk of developing asthma. The airway epithelium is first barrier to interact with, and respond to, environmental agents (pollution, viral infection, allergens), suggesting that it is a key player in the pathology of asthma. Epithelial cells play a key role in the regulation of tissue homeostasis by the modulation of numerous molecules, from antioxidants and lipid mediators to growth factors, cytokines, and chemokines. Additionally, the epithelium is also able to suppress mechanisms involved in, for example, inflammation in order to maintain homeostasis. An intrinsic alteration or defect in these regulation mechanisms compromises the epithelial barrier, and therefore, the barrier may be more prone to environmental substances and thus more likely to exhibit an asthmatic phenotype. In support of this, polymorphisms in a number of genes that are expressed in the bronchial epithelium have been linked to asthma susceptibility, while environmental factors may affect epigenetic mechanisms that can alter epithelial function and response to environmental insults. A detailed understanding of the regulatory role of the airway epithelium is required to develop new therapeutic strategies for asthma that not only address the symptoms but also the underlining pathogenic mechanism(s) and prevent airway remodelling.

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Published date: 24 March 2014

Identifiers

Local EPrints ID: 440715
URI: http://eprints.soton.ac.uk/id/eprint/440715
ISSN: 0954-7894
PURE UUID: 84f30e1d-d193-46b5-8bc2-1b07162d6587
ORCID for Matthew Loxham: ORCID iD orcid.org/0000-0001-6459-538X
ORCID for Donna Davies: ORCID iD orcid.org/0000-0002-5117-2991
ORCID for Cornelia Blume: ORCID iD orcid.org/0000-0001-6133-7318

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Date deposited: 14 May 2020 16:30
Last modified: 23 May 2020 00:34

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