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Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients

Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients
Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients
The bronchial epithelium is continuously exposed to a multitude of noxious challenges in inhaled air. Cellular contact with most damaging agents is reduced by the action of the mucociliary apparatus and by formation of a physical barrier that controls passage of ions and macromolecules. In conjunction with these defensive barrier functions, immunomodulatory cross-talk between the bronchial epithelium and tissue-resident immune cells controls the tissue microenvironment and barrier homeostasis. This is achieved by expression of an array of sensors that detect a wide variety of viral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many different soluble and cell-surface molecules that signal to cells of the immune system. The ability of the bronchial epithelium to control the balance of inhibitory and activating signals is essential for orchestrating appropriate inflammatory and immune responses and for temporally modulating these responses to limit tissue injury and control the resolution of inflammation during tissue repair. In asthmatic patients abnormalities in many aspects of epithelial barrier function have been identified. We postulate that such abnormalities play a causal role in immune dysregulation in the airways by translating gene-environment interactions that underpin disease pathogenesis and exacerbation.
0091-6749
1736-1751
Loxham, Matthew
8ef02171-9040-4c1d-8452-2ca34c56facb
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Loxham, Matthew
8ef02171-9040-4c1d-8452-2ca34c56facb
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38

Loxham, Matthew and Davies, Donna E. (2017) Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients. Journal of Allergy and Clinical Immunology, 139 (6), 1736-1751. (doi:10.1016/j.jaci.2017.04.005).

Record type: Review

Abstract

The bronchial epithelium is continuously exposed to a multitude of noxious challenges in inhaled air. Cellular contact with most damaging agents is reduced by the action of the mucociliary apparatus and by formation of a physical barrier that controls passage of ions and macromolecules. In conjunction with these defensive barrier functions, immunomodulatory cross-talk between the bronchial epithelium and tissue-resident immune cells controls the tissue microenvironment and barrier homeostasis. This is achieved by expression of an array of sensors that detect a wide variety of viral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many different soluble and cell-surface molecules that signal to cells of the immune system. The ability of the bronchial epithelium to control the balance of inhibitory and activating signals is essential for orchestrating appropriate inflammatory and immune responses and for temporally modulating these responses to limit tissue injury and control the resolution of inflammation during tissue repair. In asthmatic patients abnormalities in many aspects of epithelial barrier function have been identified. We postulate that such abnormalities play a causal role in immune dysregulation in the airways by translating gene-environment interactions that underpin disease pathogenesis and exacerbation.

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Accepted/In Press date: 14 April 2017
e-pub ahead of print date: 2 June 2017
Published date: June 2017

Identifiers

Local EPrints ID: 412359
URI: https://eprints.soton.ac.uk/id/eprint/412359
ISSN: 0091-6749
PURE UUID: be862e17-80f7-400d-a162-1e223cd3f18f
ORCID for Matthew Loxham: ORCID iD orcid.org/0000-0001-6459-538X
ORCID for Donna E. Davies: ORCID iD orcid.org/0000-0002-5117-2991

Catalogue record

Date deposited: 17 Jul 2017 13:31
Last modified: 09 Dec 2019 18:48

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