Signaling the brain in inflammation: The role of endothelial cells
Signaling the brain in inflammation: The role of endothelial cells
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DOI：
10.2741/1439
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发表时间：
2004-09-01
影响因子：
3.1
通讯作者：
Kobayashi, S
中科院分区：
文献类型：
--
作者：
Matsumura, K;Kobayashi, S
外周炎症主要通过激活的免疫细胞释放的血液传播的促炎细胞因子向大脑发出信号。除了这些细胞因子之外，已知免疫脑信号传导涉及另一种关键介质，前列腺素E-2（PGE（2）），其水平在各种炎症状态期间在脑中升高，并且其作用是影响中枢神经元活动以引起一些但不是全部的疾病行为，包括发热和下丘脑垂体-肾上腺轴的激活。过去十年的研究表明，脑内皮细胞是各种炎症状态下PGE（2）的主要来源。在这篇综述中，我们强调了内皮机制在PGE（2）介导的免疫脑信号传导中的重要性，但也讨论了其他机制对脑PGE（2）升高的可能影响。
Peripheral inflammation signals the brain primarily via blood-borne proinflammatory cytokines, released from activated immune cells. In addition to these cytokines, immune-brain signaling is known to involve another key mediator, prostaglandin E-2 (PGE(2)), the level of which is elevated in the brain during various inflammatory states and which acts to influence the central neuronal activity to evoke some, but not all, of the sickness behavior including fever and the activation of hypothalamopituitary-adrenal axis. Studies over the last decade have indicated that brain endothelial cells are the major source of PGE(2) under various inflammatory states. In this review, we highlight the significance of the endothelial mechanism in immune-brain signaling mediated by PGE(2), but discuss also the possible influence of other mechanisms on brain PGE(2) elevation.