Catecholamines induce IL-10 release in patients suffering from acute myocardial infarction by transactivating its promoter in monocytic but not in T-cells

The anti-inflammatory cytokine IL-10 is up-regulated in response to TNF-alp ha suggesting a control mechanism of inflammation. In addition, we recently found systemic IL-10 release in response to acute stress reactions in the absence of any systemic inflammation. In vitro and in vivo studies in exper imental models suggest that catecholamines induce IL-10 release via a cycli c adenosine monophosphate/protein kinase A (cAMP/PKA) dependent pathway. He re we studied patients for plasma IL-10 after acute myocardial infarction, a very stressful event without significant signs of systemic inflammation. In fact, the activation of the sympathetic system initiated by cardiac infa rction was accompanied by a temporary systemic release of IL-10. Catecholam ine induced IL-10 may be released by different cells. Recently, we demonstr ated that catecholamines directly stimulate the IL-10 promoter/enhancer via a cAMP/PKA pathway in monocytic cells. A cAMP responsive element (CRE) was identified as major target. Here we show that there is no influence of cat echolamines on the IL-10 promoter activity in T-cells. In contrast to monoc ytic cells, in T-cells cAMP-induced PKA-dependent phosphorylation of the CR E-binding protein 1 (CREB-1) seems to play a marginal role in IL-10 inducti on, which was reflected by a low cAMP-dependent IL-10-promoter/enhancer sti mulation in reporter gene assays. Thus, catecholamines are directly involve d in the regulation of IL-10 expression in monocytic but not in T-cells aft er acute stressful conditions.