Characterization of eicosanoid release in luminal, epithelial and parenchymal cells of mammalian lung
Characterization of eicosanoid release in luminal, epithelial and parenchymal cells of mammalian lung
Mediators released by cell types present in the airways have been implicated in the pathogenesis of inflammatory lung disease. This study was designed to investigate the ability of cells from mammalian lung to synthesize and release eicosanoids, and to study the possible cellular interactions which may augment such release. Initial studies showed that cells dispersed from human lung parenchyma release cyclooxygenase and lipoxygenase products of arachidonic acid in response to both calcium- and IgE-dependent activation. Experiments to investigate whether mast cells require the presence of a second cell type for maximal release of sulphidopeptide luekotrienes were performed using fractions enriched or depleted in mast cells. These experiments indicate that a second cell type is not necessary. Other experimental studies, using cells obtained by bronchoalveolar lavage of macaque monkeys, demonstrated that granulocytes and macrophages present in the lumen of primate lung can interact to give enhanced release of LTC4. Although eosinophils and macrophages were implicated in this interaction, the precise mechanism by which this enhancement occurs remains to be elucidated. The final stage of study involved an investigation of the ability of the airways epithelium to synthesize and release eicosanoids. This work was conducted using human cultured epithelial cells, and showed that the major eicosanoid generated by these cells was PGE2. This research has demonstrated that cell types in the lung are capable of the synthesis and release of an array of mediators and can participate in cellular interactions, which may then lead to the development of airways inflammation.
University of Southampton
Campbell, Alison Margaret
5af1a0ec-3d11-47f7-9b16-6f46627e9d7b
1989
Campbell, Alison Margaret
5af1a0ec-3d11-47f7-9b16-6f46627e9d7b
Campbell, Alison Margaret
(1989)
Characterization of eicosanoid release in luminal, epithelial and parenchymal cells of mammalian lung.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Mediators released by cell types present in the airways have been implicated in the pathogenesis of inflammatory lung disease. This study was designed to investigate the ability of cells from mammalian lung to synthesize and release eicosanoids, and to study the possible cellular interactions which may augment such release. Initial studies showed that cells dispersed from human lung parenchyma release cyclooxygenase and lipoxygenase products of arachidonic acid in response to both calcium- and IgE-dependent activation. Experiments to investigate whether mast cells require the presence of a second cell type for maximal release of sulphidopeptide luekotrienes were performed using fractions enriched or depleted in mast cells. These experiments indicate that a second cell type is not necessary. Other experimental studies, using cells obtained by bronchoalveolar lavage of macaque monkeys, demonstrated that granulocytes and macrophages present in the lumen of primate lung can interact to give enhanced release of LTC4. Although eosinophils and macrophages were implicated in this interaction, the precise mechanism by which this enhancement occurs remains to be elucidated. The final stage of study involved an investigation of the ability of the airways epithelium to synthesize and release eicosanoids. This work was conducted using human cultured epithelial cells, and showed that the major eicosanoid generated by these cells was PGE2. This research has demonstrated that cell types in the lung are capable of the synthesis and release of an array of mediators and can participate in cellular interactions, which may then lead to the development of airways inflammation.
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Published date: 1989
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Local EPrints ID: 458326
URI: http://eprints.soton.ac.uk/id/eprint/458326
PURE UUID: b7139efa-26e6-44d9-941f-b12175c35b3d
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Date deposited: 04 Jul 2022 16:46
Last modified: 23 Jul 2022 00:15
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Author:
Alison Margaret Campbell
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