Studies on the mechanism of adenosine-induced bronchoconstriction in asthma
Studies on the mechanism of adenosine-induced bronchoconstriction in asthma
The mechanism by which adenosine produces or enhances mediator release from mast cells is not fully understood, and direct evidence of mast cell mediator release following adenosine or AMP bronchoprovocation in man has hitherto been lacking. In this thesis, the mechanism of adenosine-induced bronchoconstriction in asthma has been further investigated in vitro and in vivo, with particular emphasis on the role of mast cell activation in this response. My studies show that if this effect is isolated to atopic and asthmatic subjects because of an increased sensitivity to modulation by adenosine and its analogues in the cells of these individuals, then this is not reflected by the responsiveness of their peripheral circulating basophils in vitro. It has also been shown that adenosine and its analogues functionally antagonise the effects of adrenergic inhibition of tonsillar mast cell activation resulting in an increase in net histamine release. Furthermore, it has been demonstrated for the first time that AMP-induced bronchoconstriction in atopic non-asthmatic and atopic and non-atopic asthmatic subjects is associated with mast cell mediator release. In summary, it is likely that adenosine-induced bronchoconstriction in asthma is accompanied by mast cell activation and this may be further exacerbated by the antagonism of adrenergic inhibition of mast cell activation, although other mechanisms may also be involved.
University of Southampton
1992
Ng, Wai Hong
(1992)
Studies on the mechanism of adenosine-induced bronchoconstriction in asthma.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
The mechanism by which adenosine produces or enhances mediator release from mast cells is not fully understood, and direct evidence of mast cell mediator release following adenosine or AMP bronchoprovocation in man has hitherto been lacking. In this thesis, the mechanism of adenosine-induced bronchoconstriction in asthma has been further investigated in vitro and in vivo, with particular emphasis on the role of mast cell activation in this response. My studies show that if this effect is isolated to atopic and asthmatic subjects because of an increased sensitivity to modulation by adenosine and its analogues in the cells of these individuals, then this is not reflected by the responsiveness of their peripheral circulating basophils in vitro. It has also been shown that adenosine and its analogues functionally antagonise the effects of adrenergic inhibition of tonsillar mast cell activation resulting in an increase in net histamine release. Furthermore, it has been demonstrated for the first time that AMP-induced bronchoconstriction in atopic non-asthmatic and atopic and non-atopic asthmatic subjects is associated with mast cell mediator release. In summary, it is likely that adenosine-induced bronchoconstriction in asthma is accompanied by mast cell activation and this may be further exacerbated by the antagonism of adrenergic inhibition of mast cell activation, although other mechanisms may also be involved.
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Published date: 1992
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Local EPrints ID: 461687
URI: http://eprints.soton.ac.uk/id/eprint/461687
PURE UUID: 45e1df44-57d8-4fc2-aa35-e95b278e4e3e
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Date deposited: 04 Jul 2022 18:52
Last modified: 04 Jul 2022 18:52
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Author:
Wai Hong Ng
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