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

• Published in: Molecular and cellular biochemistry 2000-09, Vol.212 (1-2), p.45-50
• Main Authors: Riese, U, Brenner, S, Döcke, W D, Prösch, S, Reinke, P, Oppert, M, Volk, H D, Platzer, C
• Format: Article
• Language: English
• Subjects: Acute Disease; Aged; Bucladesine - pharmacology; Catecholamines - physiology; Catecholamines - therapeutic use; Cell Line; Cyclic AMP Response Element-Binding Protein - metabolism; Epinephrine - blood; Female; Heart attacks; Humans; Interleukin-10 - blood; Interleukin-10 - genetics; Jurkat Cells; Kinases; Male; Middle Aged; Monocytes - immunology; Myocardial infarction; Myocardial Infarction - blood; Myocardial Infarction - immunology; Norepinephrine - blood; Promoter Regions, Genetic - drug effects; Shock, Cardiogenic - blood; Shock, Cardiogenic - drug therapy; Shock, Cardiogenic - immunology; T-Lymphocytes - immunology; Transcriptional Activation; Transfection
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1023/A:1007196602659

The anti-inflammatory cytokine IL-10 is up-regulated in response to TNF-alpha 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 experimental models suggest that catecholamines induce IL-10 release via a cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) dependent pathway. Here 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 infarction was accompanied by a temporary systemic release of IL-10. Catecholamine induced IL-10 may be released by different cells. Recently, we demonstrated 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 catecholamines on the IL-10 promoter activity in T-cells. In contrast to monocytic cells, in T-cells cAMP-induced PKA-dependent phosphorylation of the CRE-binding protein 1 (CREB-1) seems to play a marginal role in IL-10 induction, which was reflected by a low cAMP-dependent IL-10-promoter/enhancer stimulation in reporter gene assays. Thus, catecholamines are directly involved in the regulation of IL-10 expression in monocytic but not in T-cells after acute stressful conditions.