Divergent neuroendocrine responses to localized and systemic inflammation.

Divergent neuroendocrine responses to localized and systemic inflammation.
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DOI:
10.1016/j.smim.2014.01.004
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发表时间:
2014-10
影响因子:
7.8
通讯作者:
Lomax AE
Lomax AE
中科院分区:
医学2区
文献类型:
--
作者:
Lukewich MK;Rogers RC;Lomax AE

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交感神经系统(SNS)是损伤和感染后恢复动态平衡的综合网络的一部分。SNS可通过节后交感神经元和肾上腺嗜铬细胞(ACCs)分泌儿茶酚胺来负反馈控制炎症反应。中枢自主神经结构接收有关身体炎症状态的信息,并反射性地调节SNS活动。然而,炎症和感染也可以通过对节后细胞的外周作用直接调节SNS的功能。本综述讨论了炎症如何激活自主神经反射通路,并比较了局部炎症和全身性炎症对ACCs和节后交感神经元的影响。全身性炎症通过增加内质网钙离子的释放,显著增加儿茶酚胺的分泌。相反,急性和慢性胃肠道炎症降低了电压门控钙电流。因此,外周和全身炎症神经内分泌功能的影响机制似乎集中在细胞内钙信号的调节上。
The sympathetic nervous system (SNS) is part of an integrative network that functions to restore homeostasis following injury and infection. The SNS can provide negative feedback control over inflammation through the secretion of catecholamines from postganglionic sympathetic neurons and adrenal chromaffin cells (ACCs). Central autonomic structures receive information regarding the inflammatory status of the body and reflexively modulate SNS activity. However, inflammation and infection can also directly regulate SNS function by peripheral actions on postganglionic cells. The present review discusses how inflammation activates autonomic reflex pathways and compares the effect of localised and systemic inflammation on ACCs and postganglionic sympathetic neurons. Systemic inflammation significantly enhanced catecholamine secretion through an increase in Ca2+ release from the endoplasmic reticulum. In contrast, acute and chronic GI inflammation reduced voltage-gated Ca2+ current. Thus it appears that the mechanisms underlying the effects of peripheral and systemic inflammation neuroendocrine function converge on the modulation of intracellular Ca2+ signaling.
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