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https://hdl.handle.net/2440/27588
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Type: | Journal article |
Title: | Immunomodulatory impact of the A2A adenosine receptor on the profile of chemokines produced by neutrophils |
Author: | McColl, S. St-Onge, M. Dussault, A. Laflamme, C. Bouchard, L. Boulanger, J. Pouliot, M. |
Citation: | The FASEB Journal, 2005; 19(13):U773-U791 |
Publisher: | Federation Amer Soc Exp Biol |
Issue Date: | 2005 |
ISSN: | 0892-6638 1530-6860 |
Statement of Responsibility: | Shaun R. McColl, Mireille St-Onge, Andree-Anne Dussault, Cynthia Laflamme, Line Bouchard, Jean Boulanger, and Marc Pouliot |
Abstract: | In LPS-stimulated human neutrophils, engagement of the adenosine A2A receptor selectively prevented the expression and release of TNF-α, MIP-1α/CCL3, MIP-1β/CCL4, MIP-2α/CXCL2, and MIP-3α/CCL20. In mice lacking the A2A receptor, granulocytes that migrated into the air pouch 4 h after LPS injection expressed higher mRNA levels of TNF-α, MIP-1α, and MIP-1β than PMNs from wild-type mice. In mononuclear cells present in the air pouch 72 h after LPS injection, expression of IL-1β, TNF-α, IL-6, and MCP-2/CCL6 was higher in A2AR knockout mice. In addition to highlighting neutrophils as an early and pivotal target for mediating adenosine anti-inflammatory activities, these results identify TNF-α and the MIP chemokine family as gene products whose expression is pivotally affected by activation of A2AR in LPS-activated PMNs. Modulation by A2AR in the production of inflammatory signals by PMNs may thus influence the evolution of an inflammatory response by reducing the activation status of inflammatory cells. |
Keywords: | polymorphonuclear leukocytes experimental animal models resolution of inflammation |
Rights: | © 2005 FASEB |
DOI: | 10.1096/fj.05-4804fje |
Published version: | http://www.fasebj.org/cgi/content/abstract/05-4804fjev1 |
Appears in Collections: | Aurora harvest 2 Molecular and Biomedical Science publications |
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