Catecholamines trigger IL-10 release in acute systemic stress reaction by direct stimulation of its promoter/enhancer activity in monocytic cells.
Acute stress reactions (e.g. linked with trauma, major surgery, psychic stress and myocardial infarction) are accompanied with temporary systemic release of the anti-inflammatory cytokine IL-10 followed by immunodepression. Since an association between activation of the sympathetic system and IL-10 release has been described, we studied the influence of catecholamines on its promoter activity in vitro. Using reporter gene assays we demonstrated that catecholamines in monocytic cells directly stimulate the IL-10 promoter/enhancer via a cAMP/protein kinase A-dependent pathway. A cAMP responsive element was identified as major target. Thus, catecholamines are directly involved in the regulation of immunoresponsiveness under stressful conditions.
Platzer
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Institute of Anatomy, Anatomy II, Medical School, Friedrich Schiller University Jena, 07740, Jena, Germany. cplatzer@mti-n.uni-jena.de
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D002395:Catecholamines / Q000494:pharmacology*; D002460:Cell Line; D000242:Cyclic AMP / Q000494:pharmacology; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004742:Enhancer Elements, Genetic; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism*; D011401:Promoter Regions, Genetic; D018343:Receptors, Adrenergic, beta-2 / Q000502:physiology; D020218:Response Elements; D013312:Stress, Physiological / Q000276:immunology*
D002395:Catecholamines; D017362:Cyclic AMP Response Element-Binding Protein; D018343:Receptors, Adrenergic, beta-2; D016753:Interleukin-10; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases