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Evidence for post-transcriptional regulation of interleukin-5 by dexamethasone

Evidence for post-transcriptional regulation of interleukin-5 by dexamethasone
Evidence for post-transcriptional regulation of interleukin-5 by dexamethasone
Interleukin-5 (IL-5) is a T helper type 2 cytokine, which is implicated in the pathogenesis of eosinophilic diseases such as asthma. Both peripheral blood mononuclear cells (PBMC) and primary human T cells display similar patterns of IL-5 expression when stimulated with both phorbol-12-myristate 13-acetate and phytohaemagglutinin. The expression of IL-5 stimulated by these agents was shown to require de novo transcription and translation. However, although dexamethasone was a potent inhibitor of both IL-5 release and messenger RNA accumulation from PBMC and T cells, dexamethasone had no effect on the luciferase activity of a reporter construct under the control of an IL-5 promoter region transiently transfected into primary human T cells. Furthermore, dexamethasone appeared to decrease the stability of IL-5 messenger RNA and this effect was dependent upon de novo transcription. Taken together, the results presented here suggest that, whilst transcriptional processes predominantly regulate IL-5 release, the mechanism by which dexamethasone inhibits IL-5 is post-transcriptional
0019-2805
527-535
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Bergmann, Martin W.
569898b9-1e22-497d-964b-85bb6741f48c
Barnes, Peter J.
6cbf850c-3499-4e23-983c-4442643c0004
Newton, Robert
4a2c2a99-b7ad-4373-8840-96fbb5b5313e
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Bergmann, Martin W.
569898b9-1e22-497d-964b-85bb6741f48c
Barnes, Peter J.
6cbf850c-3499-4e23-983c-4442643c0004
Newton, Robert
4a2c2a99-b7ad-4373-8840-96fbb5b5313e

Staples, Karl J., Bergmann, Martin W., Barnes, Peter J. and Newton, Robert (2003) Evidence for post-transcriptional regulation of interleukin-5 by dexamethasone. Immunology, 109 (4), 527-535. (doi:10.1046/j.1365-2567.2003.01679.x). (PMID:12871219)

Record type: Article

Abstract

Interleukin-5 (IL-5) is a T helper type 2 cytokine, which is implicated in the pathogenesis of eosinophilic diseases such as asthma. Both peripheral blood mononuclear cells (PBMC) and primary human T cells display similar patterns of IL-5 expression when stimulated with both phorbol-12-myristate 13-acetate and phytohaemagglutinin. The expression of IL-5 stimulated by these agents was shown to require de novo transcription and translation. However, although dexamethasone was a potent inhibitor of both IL-5 release and messenger RNA accumulation from PBMC and T cells, dexamethasone had no effect on the luciferase activity of a reporter construct under the control of an IL-5 promoter region transiently transfected into primary human T cells. Furthermore, dexamethasone appeared to decrease the stability of IL-5 messenger RNA and this effect was dependent upon de novo transcription. Taken together, the results presented here suggest that, whilst transcriptional processes predominantly regulate IL-5 release, the mechanism by which dexamethasone inhibits IL-5 is post-transcriptional

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e-pub ahead of print date: 18 July 2003
Published date: August 2003
Organisations: Faculty of Medicine

Identifiers

Local EPrints ID: 374404
URI: http://eprints.soton.ac.uk/id/eprint/374404
ISSN: 0019-2805
PURE UUID: d13a26e4-f141-4fe3-8380-d4a21c482e22
ORCID for Karl J. Staples: ORCID iD orcid.org/0000-0003-3844-6457

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Date deposited: 16 Feb 2015 12:14
Last modified: 07 Aug 2019 00:40

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Contributors

Author: Karl J. Staples ORCID iD
Author: Martin W. Bergmann
Author: Peter J. Barnes
Author: Robert Newton

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