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Csóka B, Németh ZH, Selmeczy Z, et al. Role of A(2A) adenosine receptors in regulation of opsonized E. coli-induced macrophage function. Purinergic Signal. 2007;3(4):447-52doi: 10.1007/s11302-007-9075-x.
Csóka, B., Németh, Z. H., Selmeczy, Z., Koscsó, B., Pacher, P., Vizi, E. S., Deitch, E. A., & Haskó, G. (2007). Role of A(2A) adenosine receptors in regulation of opsonized E. coli-induced macrophage function. Purinergic signalling, 3(4), 447-52. https://doi.org/10.1007/s11302-007-9075-x
Csóka, Balázs, et al. "Role of A(2A) adenosine receptors in regulation of opsonized E. coli-induced macrophage function." Purinergic signalling vol. 3,4 (2007): 447-52. doi: https://doi.org/10.1007/s11302-007-9075-x
Csóka B, Németh ZH, Selmeczy Z, Koscsó B, Pacher P, Vizi ES, Deitch EA, Haskó G. Role of A(2A) adenosine receptors in regulation of opsonized E. coli-induced macrophage function. Purinergic Signal. 2007 Sep;3(4):447-52. doi: 10.1007/s11302-007-9075-x. Epub 2007 Sep 05. PMID: 18404457; PMCID: PMC2072923.
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Purinergic Signal. 2007 Sep;3(4):447-52. doi: 10.1007/s11302-007-9075-x. Epub 2007 Sep 05.

Role of A(2A) adenosine receptors in regulation of opsonized E. coli-induced macrophage function.

Purinergic signalling

Balázs Csóka, Zoltán H Németh, Zsolt Selmeczy, Balázs Koscsó, Pál Pacher, E Sylvester Vizi, Edwin A Deitch, György Haskó

Affiliations

  1. Department of Surgery, UMDNJ-New Jersey Medical School, 185 South Orange Avenue, University Heights, Newark, NJ, 07103, USA.

PMID: 18404457 PMCID: PMC2072923 DOI: 10.1007/s11302-007-9075-x

Abstract

Adenosine is a biologically active molecule that is formed at sites of metabolic stress associated with trauma and inflammation, and its systemic level reaches high concentrations in sepsis. We have recently shown that inactivation of A(2A) adenosine receptors decreases bacterial burden as well as IL-10, IL-6, and MIP-2 production in mice that were made septic by cecal ligation and puncture (CLP). Macrophages are important in both elimination of pathogens and cytokine production in sepsis. Therefore, in the present study, we questioned whether macrophages are responsible for the decreased bacterial load and cytokine production in A(2A) receptor-inactivated septic mice. We showed that A(2A) KO and WT peritoneal macrophages obtained from septic animals were equally effective in phagocytosing opsonized E. coli. IL-10 production induced by opsonized E. coli was decreased in macrophages obtained from septic A(2A) KO mice as compared to WT counterparts. In contrast, the release of IL-6 and MIP-2 induced by opsonized E. coli was higher in septic A(2A) KO macrophages than WT macrophages. These results suggest that peritoneal macrophages are not responsible for the decreased bacterial load and diminished MIP-2 and IL-6 production that are observed in septic A(2A) KO mice. In contrast, peritoneal macrophages may contribute to the suppressive effect of A(2A) receptor inactivation on IL-10 production during sepsis.

Keywords: Adenosine; Cytokines; Inflammation; Macrophages; Phagocytosis; Sepsis

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