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The bronchial epithelium in asthma--much more than a passive barrier

The bronchial epithelium in asthma--much more than a passive barrier
The bronchial epithelium in asthma--much more than a passive barrier
The bronchial epithelium has a multifunctional role in the airway. It is actively engaged in communicating with cells of the immune and inflammatory systems, as well as secreting cytoprotective molecules and acting as a physical barrier between the internal and external milieu of the lungs. In asthma, the bronchial epithelium is often damaged, with shedding of the columnar cells into the airway lumen. This damage and ensuing repair responses are proposed to orchestrate airway remodelling via activation of myofibroblasts in the underlying lamina reticularis. This allows the two cell types to work as a trophic unit, propagating and amplifying the response at the cell surface into the submucosa. In addition to structural damage, the epithelium displays an "activated" phenotype evident by activation of transcription factors such as nuclear factor kappa B (NF kappa B), and expression of mediators which directly or indirectly lead to a chronic cycle of inflammation and injury. A diverse number of innocuous stimuli trigger asthma. It is likely that interactions between genetic and environmental factors converge on common intracellular signalling pathways that regulate epithelial stress and repair. Of particular relevance is the NF kappa B signalling pathway and the mitogen activated protein kinase pathways (MAPKs), of which the mitogen activated extracellular regulated kinases (ERKs), and the stress activated P38 and c-Jun NH2 terminal kinase (JNKs) are best known. This review aims to highlight the importance of these signalling pathways in coordinating the response to diverse stimuli at the surface of the bronchial epithelium which leads to development and maintenance of the asthmatic state.
1122-0643
48-54
Hamilton, L.M.
8ff57fe6-ea6d-4d13-9245-695e828c0034
Davies, D.E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Wilson, S.J.
21c6875d-6870-441b-ae7a-603562a646b8
Kimber, I.
c740b0a8-694f-40bb-993e-f10b9a557c5f
Dearman, R.J.
f6695810-c848-403d-9d9e-523719441f35
Holgate, S.T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc
Hamilton, L.M.
8ff57fe6-ea6d-4d13-9245-695e828c0034
Davies, D.E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Wilson, S.J.
21c6875d-6870-441b-ae7a-603562a646b8
Kimber, I.
c740b0a8-694f-40bb-993e-f10b9a557c5f
Dearman, R.J.
f6695810-c848-403d-9d9e-523719441f35
Holgate, S.T.
2e7c17a9-6796-436e-8772-1fe6d2ac5edc

Hamilton, L.M., Davies, D.E., Wilson, S.J., Kimber, I., Dearman, R.J. and Holgate, S.T. (2001) The bronchial epithelium in asthma--much more than a passive barrier. Monaldi Archives for Chest Disease, 56 (1), 48-54.

Record type: Article

Abstract

The bronchial epithelium has a multifunctional role in the airway. It is actively engaged in communicating with cells of the immune and inflammatory systems, as well as secreting cytoprotective molecules and acting as a physical barrier between the internal and external milieu of the lungs. In asthma, the bronchial epithelium is often damaged, with shedding of the columnar cells into the airway lumen. This damage and ensuing repair responses are proposed to orchestrate airway remodelling via activation of myofibroblasts in the underlying lamina reticularis. This allows the two cell types to work as a trophic unit, propagating and amplifying the response at the cell surface into the submucosa. In addition to structural damage, the epithelium displays an "activated" phenotype evident by activation of transcription factors such as nuclear factor kappa B (NF kappa B), and expression of mediators which directly or indirectly lead to a chronic cycle of inflammation and injury. A diverse number of innocuous stimuli trigger asthma. It is likely that interactions between genetic and environmental factors converge on common intracellular signalling pathways that regulate epithelial stress and repair. Of particular relevance is the NF kappa B signalling pathway and the mitogen activated protein kinase pathways (MAPKs), of which the mitogen activated extracellular regulated kinases (ERKs), and the stress activated P38 and c-Jun NH2 terminal kinase (JNKs) are best known. This review aims to highlight the importance of these signalling pathways in coordinating the response to diverse stimuli at the surface of the bronchial epithelium which leads to development and maintenance of the asthmatic state.

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Published date: 2001

Identifiers

Local EPrints ID: 27086
URI: https://eprints.soton.ac.uk/id/eprint/27086
ISSN: 1122-0643
PURE UUID: f6709785-e141-4b4b-9bcc-8e25a6818d3a
ORCID for D.E. Davies: ORCID iD orcid.org/0000-0002-5117-2991

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Date deposited: 26 Apr 2006
Last modified: 24 May 2019 00:39

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