The effect of respiratory viral infections on human circulatory leukocytes
The effect of respiratory viral infections on human circulatory leukocytes
We have investigated the effect of community-acquired respiratory infections on human circulatory leukocytes. A cohort of asthmatic subjects and their non-asthmatic spouses were studied for 1 year. Blood samples were collected when donors experienced cold symptoms and again 2-3 weeks later. We found that there was a small but significant increase in the number of peripheral blood neutrophils during a symptomatic episode; however, the levels of eosinophils did not change. Basophil histamine and leukotriene release to anti-IgE (an artificial allergen) was increased during colds, in both asthmatic and non-asthmatic subjects. Also, mediator release caused by clustering the basophil surface integrins CD29 and CD 49d (which mimics cell adhesion) was increased during a symptomatic episode. Further, this effect tended to be more pronounced in asthmatic donors. However, respiratory illness did not alter spontaneous histamine release, indicating that general responsiveness was not changed.
Since respiratory tract infections can have systemic consequences, indirect mechanisms for these effects are likely. Cytokines represent candidate signalling molecules, and many are known to be induced or increased in asthma and by viruses. We looked at the effects of interleukin (IL)-11 (a newly-appreciated virus-induced cytokine) on aspects of leukocyte function, and compared its effects with γ-interferon (IFN) and IL-8. We have found that IL-8 and γ-IFN, but not IL-11, enhanced anti-IgE induced basophil histamine release. None of the cytokines affected neutrophil superoxide production.
University of Southampton
Thomas, Lynette Hazel
99dbb842-a8b8-4787-9ff0-f83d75a572ca
1996
Thomas, Lynette Hazel
99dbb842-a8b8-4787-9ff0-f83d75a572ca
Thomas, Lynette Hazel
(1996)
The effect of respiratory viral infections on human circulatory leukocytes.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
We have investigated the effect of community-acquired respiratory infections on human circulatory leukocytes. A cohort of asthmatic subjects and their non-asthmatic spouses were studied for 1 year. Blood samples were collected when donors experienced cold symptoms and again 2-3 weeks later. We found that there was a small but significant increase in the number of peripheral blood neutrophils during a symptomatic episode; however, the levels of eosinophils did not change. Basophil histamine and leukotriene release to anti-IgE (an artificial allergen) was increased during colds, in both asthmatic and non-asthmatic subjects. Also, mediator release caused by clustering the basophil surface integrins CD29 and CD 49d (which mimics cell adhesion) was increased during a symptomatic episode. Further, this effect tended to be more pronounced in asthmatic donors. However, respiratory illness did not alter spontaneous histamine release, indicating that general responsiveness was not changed.
Since respiratory tract infections can have systemic consequences, indirect mechanisms for these effects are likely. Cytokines represent candidate signalling molecules, and many are known to be induced or increased in asthma and by viruses. We looked at the effects of interleukin (IL)-11 (a newly-appreciated virus-induced cytokine) on aspects of leukocyte function, and compared its effects with γ-interferon (IFN) and IL-8. We have found that IL-8 and γ-IFN, but not IL-11, enhanced anti-IgE induced basophil histamine release. None of the cytokines affected neutrophil superoxide production.
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Published date: 1996
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Local EPrints ID: 459956
URI: http://eprints.soton.ac.uk/id/eprint/459956
PURE UUID: 78f91ef1-f713-4975-9974-de356e01edf2
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Date deposited: 04 Jul 2022 17:29
Last modified: 23 Jul 2022 00:58
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Author:
Lynette Hazel Thomas
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