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|Title:||The bronchial epithelium as a target for inflammatory attack in asthma|
Holgate, Stephen T.
Herbert, Carolyn A.
Cell adhesion molecules
|Publisher:||John Wiley & Sons Ltd.|
|Citation:||Montefort, S., Herbert, C. A., Robinson, C., & Holgate, S. T. (1992). The bronchial epithelium as a target for inflammatory attack in asthma. Clinical & Experimental Allergy, 22(5), 511-520.|
|Abstract:||It has long been known that epithelial damage and shedding have been associated with the pathogenesis of bronchial asthma. More recently it has been suggested that epithelial denudation is related to the observed increase in bronchial responsiveness that is characteristic of asthma. Possible mechanisms include stimulation of exposed intraepithelial nerves leading to release of bronchoconstrictor neuropeptides . decreased production of an epithelial cell-derived relaxant factor[s] [2.3] and the production of potentially pro-inflammatory mediators such as LTB4 [4.5] and endothelin (6] from the epithelium itself. Damage to the epithelium also leads to a breakdown in the permeability barrier for both large and small molecules, loss of homeostatic control over the composition of the periciliary fluid and disruption of the mucociliary escalator.|
|Description:||The authors acknowledge grant support from the Medical Research Council, British Lung Foundation and Eli Lilly. They would also like to thank Dr D. Garrod for kindly donating some of the monoclonal antibodies used and Ms J. Baker and the staff at the Southampton General Hospital electronmicroscopy unit for their technical assistance.|
|Appears in Collections:||Scholarly Works - FacM&SMed|
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