Flierl Michael A, Rittirsch Daniel, Huber-Lang Markus, Sarma J Vidya, Ward Peter A
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-0602, USA.
Mol Med. 2008 Mar-Apr;14(3-4):195-204. doi: 10.2119/2007-00105.Flierl.
It is well established that catecholamines (CAs), which regulate immune and inflammatory responses, derive from the adrenal medulla and from presynaptic neurons. Recent studies reveal that T cells also can synthesize and release catecholamines which then can regulate T cell function. We have shown recently that macrophages and neutrophils, when stimulated, can generate and release catecholamines de novo which, then, in an autocrine/paracrine manner, regulate mediator release from these phagocytes via engagement of adrenergic receptors. Moreover, regulation of catecholamine-generating enzymes as well as degrading enzymes clearly alter the inflammatory response of phagocytes, such as the release of proinflammatory mediators. Accordingly, it appears that phagocytic cells and lymphocytes may represent a major, newly recognized source of catecholamines that regulate inflammatory responses.
众所周知,调节免疫和炎症反应的儿茶酚胺(CAs)来源于肾上腺髓质和突触前神经元。最近的研究表明,T细胞也能合成和释放儿茶酚胺,进而调节T细胞功能。我们最近发现,巨噬细胞和中性粒细胞在受到刺激时能够从头合成并释放儿茶酚胺,然后通过肾上腺素能受体的结合,以自分泌/旁分泌的方式调节这些吞噬细胞释放介质。此外,儿茶酚胺生成酶以及降解酶的调节明显改变了吞噬细胞的炎症反应,如促炎介质的释放。因此,吞噬细胞和淋巴细胞似乎可能是调节炎症反应的儿茶酚胺的一个主要的、新发现的来源。