Pulmonary surfactant and asthma
Pulmonary surfactant and asthma
Emerging evidence suggests that surfactant dysfunction, together with mediator-induced bronchoconstriction and airway oedema, may contribute to the airway obstruction characteristic of asthma. Allergen-challenged animal models have been demonstrated to develop surfactant dysfunction with an increase in airway resistance which can be prevented and partly reversed by the administration of exogenous surfactant. However there have to date been no detailed studies of surfactant composition and function in human asthma.
Pulmonary surfactant was measured in bronchoalveolar lavage fluid (BALf) and induced sputum from adults with stable asthma and healthy control subjects, and analysed for phospholipid and protein compositions and surface tension function. Phospholipid molecular species and classes were measured by electrospray mass spectrometry and surface tension function was evaluated with a capillary surfactometer.
The results of this study was that for asthmatic subjects, the proportion of dipalmitoyl phosphatidylcholine (16:0/16:0PC) decreased in sputum (p<0.05), but not in BALf. In BALf, mole% 16:0/oPC correlated with surfactant’s ability to maintain airway patency, and sputum mole % 16:0/16:0PC correlated with lung function (FEV1). Neither surfactant protein-A or total protein concentration in either BALf or sputum was altered in asthma. These results suggest altered phospholipid composition and function of airway (sputum) but not alveolar (BALf) surfactant in stable asthma. Such marginal surfactant dysfunction may predispose asthmatic subjects to further surfactant inhibition by proteins or aeroallergens in acute asthma episodes, and contribute to the loss of airway patency characteristic of asthma. Consequently, administration of an appropriate therapeutic surfactant could provide clinical benefit in asthma.
University of Southampton
Hockey, Peter Morey
d50ec5fc-512e-488a-9e8e-0a70c2682a0f
2000
Hockey, Peter Morey
d50ec5fc-512e-488a-9e8e-0a70c2682a0f
Hockey, Peter Morey
(2000)
Pulmonary surfactant and asthma.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Emerging evidence suggests that surfactant dysfunction, together with mediator-induced bronchoconstriction and airway oedema, may contribute to the airway obstruction characteristic of asthma. Allergen-challenged animal models have been demonstrated to develop surfactant dysfunction with an increase in airway resistance which can be prevented and partly reversed by the administration of exogenous surfactant. However there have to date been no detailed studies of surfactant composition and function in human asthma.
Pulmonary surfactant was measured in bronchoalveolar lavage fluid (BALf) and induced sputum from adults with stable asthma and healthy control subjects, and analysed for phospholipid and protein compositions and surface tension function. Phospholipid molecular species and classes were measured by electrospray mass spectrometry and surface tension function was evaluated with a capillary surfactometer.
The results of this study was that for asthmatic subjects, the proportion of dipalmitoyl phosphatidylcholine (16:0/16:0PC) decreased in sputum (p<0.05), but not in BALf. In BALf, mole% 16:0/oPC correlated with surfactant’s ability to maintain airway patency, and sputum mole % 16:0/16:0PC correlated with lung function (FEV1). Neither surfactant protein-A or total protein concentration in either BALf or sputum was altered in asthma. These results suggest altered phospholipid composition and function of airway (sputum) but not alveolar (BALf) surfactant in stable asthma. Such marginal surfactant dysfunction may predispose asthmatic subjects to further surfactant inhibition by proteins or aeroallergens in acute asthma episodes, and contribute to the loss of airway patency characteristic of asthma. Consequently, administration of an appropriate therapeutic surfactant could provide clinical benefit in asthma.
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Published date: 2000
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Local EPrints ID: 464946
URI: http://eprints.soton.ac.uk/id/eprint/464946
PURE UUID: 2d77370c-2c9c-4e17-a3e1-68b5f5f3dfc5
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Date deposited: 05 Jul 2022 00:13
Last modified: 23 Jul 2022 02:15
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Author:
Peter Morey Hockey
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