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Invited lecture: activation of the epithelial mesenchymal trophic unit in the pathogenesis of asthma

Invited lecture: activation of the epithelial mesenchymal trophic unit in the pathogenesis of asthma
Invited lecture: activation of the epithelial mesenchymal trophic unit in the pathogenesis of asthma
Background: A recent NIH Workshop and an ERS Task Force concluded that more work was needed to understand mechanisms of severe and chronic asthma. This report describes a series of studies that identify aberrant epithelial mesenchymal signalling in the airways as an important event in maintaining inflammation and driving remodelling in response to environmental injury. Methods: Immunohistochemistry, genotyping and functional studies conducted on cultured asthmatic cells and mucosal biopsies were used to identify biochemical pathways involved in epithelial injury and repair in asthma and their relationship to disease severity. Results: Our findings suggest that the asthmatic state results from an interaction between a susceptible epithelium and Th-2-mediated inflammation to alter the communication between the epithelium and the underlying mesenchyme - the epithelial mesenchymal trophic unit - leading to disease persistence, airway remodelling and refractoriness to corticosteroid treatment. Conclusions: Asthma is more than an inflammatory disorder, but requires engagement of important signalling pathways involved in epithelial repair and tissue remodelling. These pathways involving EGFRs and TGF-Rs provide targets against which to develop novel therapies for chronic asthma.
1018-2438
253-258
Holgate, S.T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Lackie, P.M.
4afbbe1a-22a6-4ceb-8cad-f3696dc43a7a
Howarth, P.H.
ff19c8c4-86b0-4a88-8f76-b3d87f142a21
Roche, W.R.
a5135b2d-cab5-481b-887a-78611fa00bff
Puddicombe, S.M.
5537d529-f9f2-4e37-ad10-71fae0bb8523
Richter, A.
080ff20b-2ec5-4204-a809-2d1c63e4be1f
Wilson, S.J.
21c6875d-6870-441b-ae7a-603562a646b8
Holloway, J.W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Davies, D.E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Holgate, S.T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Lackie, P.M.
4afbbe1a-22a6-4ceb-8cad-f3696dc43a7a
Howarth, P.H.
ff19c8c4-86b0-4a88-8f76-b3d87f142a21
Roche, W.R.
a5135b2d-cab5-481b-887a-78611fa00bff
Puddicombe, S.M.
5537d529-f9f2-4e37-ad10-71fae0bb8523
Richter, A.
080ff20b-2ec5-4204-a809-2d1c63e4be1f
Wilson, S.J.
21c6875d-6870-441b-ae7a-603562a646b8
Holloway, J.W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Davies, D.E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38

Holgate, S.T., Lackie, P.M., Howarth, P.H., Roche, W.R., Puddicombe, S.M., Richter, A., Wilson, S.J., Holloway, J.W. and Davies, D.E. (2001) Invited lecture: activation of the epithelial mesenchymal trophic unit in the pathogenesis of asthma. International Archives of Allergy and Immunology, 124 (1-3), 253-258. (doi:10.1159/000053726).

Record type: Article

Abstract

Background: A recent NIH Workshop and an ERS Task Force concluded that more work was needed to understand mechanisms of severe and chronic asthma. This report describes a series of studies that identify aberrant epithelial mesenchymal signalling in the airways as an important event in maintaining inflammation and driving remodelling in response to environmental injury. Methods: Immunohistochemistry, genotyping and functional studies conducted on cultured asthmatic cells and mucosal biopsies were used to identify biochemical pathways involved in epithelial injury and repair in asthma and their relationship to disease severity. Results: Our findings suggest that the asthmatic state results from an interaction between a susceptible epithelium and Th-2-mediated inflammation to alter the communication between the epithelium and the underlying mesenchyme - the epithelial mesenchymal trophic unit - leading to disease persistence, airway remodelling and refractoriness to corticosteroid treatment. Conclusions: Asthma is more than an inflammatory disorder, but requires engagement of important signalling pathways involved in epithelial repair and tissue remodelling. These pathways involving EGFRs and TGF-Rs provide targets against which to develop novel therapies for chronic asthma.

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Published date: 2001

Identifiers

Local EPrints ID: 27104
URI: https://eprints.soton.ac.uk/id/eprint/27104
ISSN: 1018-2438
PURE UUID: 5eed873e-7d69-43ee-994c-82c62231d98e
ORCID for P.M. Lackie: ORCID iD orcid.org/0000-0001-7138-3764
ORCID for J.W. Holloway: ORCID iD orcid.org/0000-0001-9998-0464
ORCID for D.E. Davies: ORCID iD orcid.org/0000-0002-5117-2991

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Date deposited: 26 Apr 2006
Last modified: 15 Aug 2019 00:58

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