The rise and fall of platelet-activating factor as a mediator of asthma
The rise and fall of platelet-activating factor as a mediator of asthma
Platelet-activating factor (PAF) has been proposed as a central inflammatory mediator in asthma. It is a potent bronchoconstrictor agent, and induces persistent bronchial heperresponsiveness in animal models. Eosinophils are chemoattracted by PAF, and are themselves major sources of PAF. The 'PAF hypothesis' proposes that PAF over-production, possibly by eosinophils, perpetuates the eosinophilia and bronchial hyperresponsiveness that are cardinal features of asthma. However, inhaled PAF does not appear to cause a specific eosinophil influx into the human lung and does not reproducibly cause bronchial hyperresponsiveness in man. Measurements of PAF in biological fluids are difficult to interpret and over-production of PAF has never been convincingly demonstrated in asthma. Potent and specific PAF antagonists have failed to block bronchoconstrictor responses and bronchial hyperrresponsiveness after inhaled allergen challenge. Trials of PAF antagonists in clinical asthma have failed to show any improvements in lung function, symptoms, bronchial responsiveness, use of rescue medication, or quality of life. The concept that PAF has a role in the pathophysiology of asthma is no longer realistically tenable, but the episode may provide instructive lessons for future research.
117-124
Sampson, A. P.
4ca76f6f-ff35-425d-a7e7-c2bd2ea2df60
1996
Sampson, A. P.
4ca76f6f-ff35-425d-a7e7-c2bd2ea2df60
Sampson, A. P.
(1996)
The rise and fall of platelet-activating factor as a mediator of asthma.
International Review of Allergology and Clinical Immunology, 2 (4), .
Abstract
Platelet-activating factor (PAF) has been proposed as a central inflammatory mediator in asthma. It is a potent bronchoconstrictor agent, and induces persistent bronchial heperresponsiveness in animal models. Eosinophils are chemoattracted by PAF, and are themselves major sources of PAF. The 'PAF hypothesis' proposes that PAF over-production, possibly by eosinophils, perpetuates the eosinophilia and bronchial hyperresponsiveness that are cardinal features of asthma. However, inhaled PAF does not appear to cause a specific eosinophil influx into the human lung and does not reproducibly cause bronchial hyperresponsiveness in man. Measurements of PAF in biological fluids are difficult to interpret and over-production of PAF has never been convincingly demonstrated in asthma. Potent and specific PAF antagonists have failed to block bronchoconstrictor responses and bronchial hyperrresponsiveness after inhaled allergen challenge. Trials of PAF antagonists in clinical asthma have failed to show any improvements in lung function, symptoms, bronchial responsiveness, use of rescue medication, or quality of life. The concept that PAF has a role in the pathophysiology of asthma is no longer realistically tenable, but the episode may provide instructive lessons for future research.
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Published date: 1996
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Copyright 2004 Elsevier Science B.V., Amsterdam. All rights reserved.
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Local EPrints ID: 455210
URI: http://eprints.soton.ac.uk/id/eprint/455210
ISSN: 1232-9142
PURE UUID: c5cde206-8875-47f7-a04b-45ce3e9f43a8
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Date deposited: 15 Mar 2022 17:34
Last modified: 03 Jun 2023 01:33
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