Immunopharmacological studies on human mast cells and basophils
Immunopharmacological studies on human mast cells and basophils
The aims of this project were first to investigate the extent to which drugs used for the treatment of allergic diseases may have an effect on the early phase of IgE-dependent mast cell activation. Second, as IL-3, some eosinophil granule proteins and histamine-releasing factors are considered to initiate basophil activation in the late phase of allergic reaction, the effect of these agents on histamine release from human mast cells was investigated. Third, the production of cytokines by human mast cells was investigated.
High concentrations of sodium cromoglycate, nedocromil sodium and antihistamines were required to significantly inhibit IgE-dependent release of histamine and PGD2 from mast cells. There was some heterogeneity observed for mast cells from different human tissues in the degree of pharmacological control by these agents. In contrast, nanomolar concentrations of β-adrenoceptor agonists consistently inhibited histamine and PGD_2 release. IL-3, eosinophil granule proteins and peripheral blood mononuclear cell-derived histamine-releasing factors neither induced nor primed IgE-dependent histamine release from human mast cells. As a part of these studies, the mechanisms of activation of basophils by IL-3 were investigated. Histamine release by IL-3 required both extracellular Ca^2+ and the presence of membrane IgE, but IL-3 priming did not. The activation of stem cell factor-primed mast cells via Fc_6RI, induced expression of IL-4 and IL-5 mRNA at time points ranging from 2 to 24 h and 2 to 72 h, respectively. In conclusion, (1) antiallergic drugs are weak inhibitors of histamine and PGD_2 release from mast cells in vitro; (2) several basophil priming factors are without effect on the functional activity of mast cells; (3) human mast cells may contribute to the chronicity of tissue inflammation by the production of cytokines.
University of Southampton
Okayama, Yoshimichi
072adc30-6081-4d59-97a7-63a2a8ca5c87
1994
Okayama, Yoshimichi
072adc30-6081-4d59-97a7-63a2a8ca5c87
Okayama, Yoshimichi
(1994)
Immunopharmacological studies on human mast cells and basophils.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
The aims of this project were first to investigate the extent to which drugs used for the treatment of allergic diseases may have an effect on the early phase of IgE-dependent mast cell activation. Second, as IL-3, some eosinophil granule proteins and histamine-releasing factors are considered to initiate basophil activation in the late phase of allergic reaction, the effect of these agents on histamine release from human mast cells was investigated. Third, the production of cytokines by human mast cells was investigated.
High concentrations of sodium cromoglycate, nedocromil sodium and antihistamines were required to significantly inhibit IgE-dependent release of histamine and PGD2 from mast cells. There was some heterogeneity observed for mast cells from different human tissues in the degree of pharmacological control by these agents. In contrast, nanomolar concentrations of β-adrenoceptor agonists consistently inhibited histamine and PGD_2 release. IL-3, eosinophil granule proteins and peripheral blood mononuclear cell-derived histamine-releasing factors neither induced nor primed IgE-dependent histamine release from human mast cells. As a part of these studies, the mechanisms of activation of basophils by IL-3 were investigated. Histamine release by IL-3 required both extracellular Ca^2+ and the presence of membrane IgE, but IL-3 priming did not. The activation of stem cell factor-primed mast cells via Fc_6RI, induced expression of IL-4 and IL-5 mRNA at time points ranging from 2 to 24 h and 2 to 72 h, respectively. In conclusion, (1) antiallergic drugs are weak inhibitors of histamine and PGD_2 release from mast cells in vitro; (2) several basophil priming factors are without effect on the functional activity of mast cells; (3) human mast cells may contribute to the chronicity of tissue inflammation by the production of cytokines.
This record has no associated files available for download.
More information
Published date: 1994
Identifiers
Local EPrints ID: 462752
URI: http://eprints.soton.ac.uk/id/eprint/462752
PURE UUID: 61fdd2e4-a0ca-4ac1-80d6-645f17310f2a
Catalogue record
Date deposited: 04 Jul 2022 19:51
Last modified: 23 Jul 2022 01:08
Export record
Contributors
Author:
Yoshimichi Okayama
Download statistics
Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.
View more statistics