| Literature DB >> 16280366 |
Shaun R McColl1, Mireille St-Onge, Andrée-Anne Dussault, Cynthia Laflamme, Line Bouchard, Jean Boulanger, Marc Pouliot.
Abstract
In LPS-stimulated human neutrophils, engagement of the adenosine A2A receptor selectively prevented the expression and release of TNF-alpha, MIP-1alpha/CCL3, MIP-1beta/CCL4, MIP-2alpha/CXCL2, and MIP-3alpha/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-alpha, MIP-1alpha, and MIP-1beta than PMNs from wild-type mice. In mononuclear cells present in the air pouch 72 h after LPS injection, expression of IL-1beta, TNF-alpha, 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-alpha 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.Entities:
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Year: 2005 PMID： 16280366 PMCID： PMC2881301 DOI： 10.1096/fj.05-4804fje
Source DB: PubMed Journal: FASEB J ISSN： 0892-6638 Impact factor: 5.191