HMGB1 as a late mediator of lethal systemic inflammation
HMGB1 as a late mediator of lethal systemic inflammation
复制标题
DOI：
10.1164/ajrccm.164.10.2106117
复制
发表时间：
2001-11-15
影响因子：
24.7
通讯作者：
Tracey, KJ
中科院分区：
文献类型：
--
作者：
Wang, HH;Yang, H;Tracey, KJ
最新技术水平1769抑制创伤患者（27）。新的证据表明，中枢神经系统可通过向组织驻留巨噬细胞发出传出迷走神经信号，直接且快速地减弱TNF对内毒素的反应（28）。这种作用是由乙酰胆碱介导的，乙酰胆碱是迷走神经的主要神经递质，通过巨噬细胞上的烟碱胆碱能受体发出信号（28）。因此，脓毒症患者中复杂的细胞因子环境的特征在于由神经和体液途径紧密调节的炎症反应和潜在的有害促炎反应之间的相互作用。
State of the Art 1769 suppressed trauma patients (27). New evidence suggests that the central nervous system can directly, and rapidly, attenuate the TNF response to endotoxin through efferent vagus nerve signals to tissue-resident macrophages (28). This effect is mediated by acetylcholine, the principal neurotransmitter of the vagus nerve, which signals via nicotinic cholinergic receptors present on macrophages (28). Thus, the complex cytokine milieu in septic patients is characterized by the interaction between antiinflammatory responses and potentially injurious proinflammatory responses that are tightly regulated by neural and humoral pathways.