Immunomodulatory impact of the A2A adenosine receptor on the profile of chemokines produced by neutrophils

被引：89

作者：

McColl, SR

St-Onge, M

Dussault, AA

Laflamme, C

Bouchard, L

Boulanger, J

Pouliot, M

机构：

[1] CHUL, Ctr Rech Rhumatol & Immunol, CHUQ, Ste Foy, PQ G1V 4G2, Canada

[2] Univ Laval, Dept Anat Physiol, Fac Med, Quebec City, PQ G1K 7P4, Canada

[3] Univ Adelaide, Sch Mol & Biomed Sci, Adelaide, SA, Australia

来源：

FASEB JOURNAL | 2005年 / 19卷 / 13期

基金：

加拿大健康研究院;

关键词：

polymorphonuclear leukocytes; experimental animal models; resolution of inflammation;

D O I：

10.1096/fj.05-4804fje

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In LPS-stimulated human neutrophils, engagement of the adenosine A(2A) receptor selectively prevented the expression and release of TNF-alpha, MIP-1 alpha/CCL3, MIP-1 beta/CCL4, MIP-2 alpha/CXCL2, and MIP-3 alpha/CCL20. In mice lacking the A(2A) receptor, granulocytes that migrated into the air pouch 4 h after LPS injection expressed higher mRNA levels of TNF-alpha, MIP-1 alpha, and MIP-1 beta than PMNs from wild-type mice. In mononuclear cells present in the air pouch 72 h after LPS injection, expression of IL-1 beta, TNF-alpha, IL- 6, and MCP-2/CCL6 was higher in A(2A)R 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 A(2A)R in LPS-activated PMNs. Modulation by A(2A)R 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.

引用

页码：187 / +

页数：19

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[11] Resident cell chemokine expression serves as the major mechanism for leukocyte recruitment during local inflammation [J].