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-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.
Riese
U
U
Institute of Anatomy II, Medical School, Friedrich Schiller University, Jena, Germany.
Brenner
S
S
Döcke
W D
WD
Prösch
S
S
Reinke
P
P
Oppert
M
M
Volk
H D
HD
Platzer
C
C
D000208:Acute Disease; D000368:Aged; D003994:Bucladesine / Q000494:pharmacology; D002395:Catecholamines / Q000502:physiology* / Q000627:therapeutic use; D002460:Cell Line; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism*; D004837:Epinephrine / Q000097:blood; D005260:Female; D006801:Humans; D016753:Interleukin-10 / Q000097:blood / Q000235:genetics*; D019169:Jurkat Cells; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D009203:Myocardial Infarction / Q000097:blood / Q000276:immunology*; D009638:Norepinephrine / Q000097:blood; D011401:Promoter Regions, Genetic / Q000187:drug effects*; D012770:Shock, Cardiogenic / Q000097:blood / Q000188:drug therapy / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D015533:Transcriptional Activation; D014162:Transfection
D002395:Catecholamines; D017362:Cyclic AMP Response Element-Binding Protein; D016753:Interleukin-10; D003994:Bucladesine; D009638:Norepinephrine; D004837:Epinephrine