多微生物败血症后骨髓祖细胞来源巨噬细胞中细胞因子释放的肾上腺素能调节

Adrenergic modulation of cytokine release in bone marrow progenitor-derived macrophage following polymicrobial sepsis.

作者信息

Muthu Kuzhali, Deng Jiangping, Gamelli Richard, Shankar Ravi, Jones Stephen B

机构信息

Department of Physiology, The Burn and Shock Trauma Institute, Loyola University Medical Center, 2160 South First Ave, Maywood, IL 60153, USA.

出版信息

J Neuroimmunol. 2005 Jan;158(1-2):50-7. doi: 10.1016/j.jneuroim.2004.08.003.

DOI:10.1016/j.jneuroim.2004.08.003

PMID:15589037

Abstract

Catecholamines may impact on the pathophysiology of sepsis by attenuating proinflammatory cytokine and augmenting antiinflammatory cytokine production by macrophages. We tested this premise in bone marrow monocyte progenitor-derived macrophages. Polymicrobial sepsis was induced in mice through cecal ligation and puncture. ER-MP 12 monocyte progenitors were isolated and differentiated into macrophages in vitro 72 hr later. Lipopolysaccharide (LPS)-stimulated cytokine production was measured with and without epinephrine, IL-10 and anti-IL-10 antibody. Epinephrine significantly increased IL-10 production, but attenuated TNF-alpha release exclusively through beta2 adrenergic receptors, and is independent of IL-10 production. Together, these results suggest that epinephrine can promote a potent antiinflammatory response in sepsis.

摘要

儿茶酚胺可能通过减弱促炎细胞因子并增强巨噬细胞产生抗炎细胞因子来影响脓毒症的病理生理学。我们在骨髓单核细胞祖细胞衍生的巨噬细胞中验证了这一假设。通过盲肠结扎和穿刺在小鼠中诱导多微生物脓毒症。分离出ER-MP 12单核细胞祖细胞，72小时后在体外将其分化为巨噬细胞。在有和没有肾上腺素、IL-10和抗IL-10抗体的情况下，测量脂多糖（LPS）刺激的细胞因子产生。肾上腺素显著增加IL-10的产生，但仅通过β2肾上腺素能受体减弱TNF-α的释放，且与IL-10的产生无关。总之，这些结果表明肾上腺素可促进脓毒症中有效的抗炎反应。