Prostaglandin E2 in the pathogenesis of fever -: An update
Prostaglandin E2 in the pathogenesis of fever -: An update
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DOI：
10.1111/j.1749-6632.1998.tb08315.x
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发表时间：
1998-01-01
期刊：
影响因子：
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通讯作者：
Akarsu, ES
中科院分区：
文献类型：
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作者：
Coceani, F;Akarsu, ES
前列腺素 E-2 (PGE(2)) 被认为是导致发烧的一系列事件中的关键中间体。通常在大脑中检测不到或几乎检测不到，它会在暴露于传染性诺拉病毒以及随之而来的外部热原性细胞因子的产生以及脑内（对于白细胞介素（IL）-6）的情况下选择性升高。循环中的热原促进脑内PGE（2）出现的机制尚不清楚，并且不知道PGE（2）激活如何选择性地随着IL-6在脑中诱导而升高。我们发现脑微血管系统不适合作为 PGE(2) 的来源来响应血源性热原。此外，我们表明 IL-6 与其他热原的不同之处在于能够特异性刺激 PGE(2) 合成。尽管如此，脑源性 IL-6 似乎并不是 PGE(2) 激活和随之而来的发烧所必需的。我们得出结论，跨血脑屏障运作的信号转导机制对于发热的发生至关重要。对全身性诺沙的反应。
Prostaglandin E-2 (PGE(2)) is recognized as a key intermediate in the sequence of events leading to fever. Normally undetectable or barely detectable in brain, it rises selectively on exposure to an infectious nora and the attendant generation of pyrogenic cytokines outside and, in the case of interleukin (IL)-6, inside the brain, The mechanism by which pyrogens in the circulation promote the appearance of PGE(2) within the confines of brain is not clear, and it is not known how PGE(2) activation is selective with IL-6 being induced in brain. We have found that the cerebral microvasculature is not suitable as a source of PGE(2) in response to blood-borne pyrogens, In addition, we show that IL-6 differs from other pyrogens in being able to stimulate specifically PGE(2) synthesis, Nevertheless, brain-derived IL-6 does not appear to be necessary for PGE(2) activation and the attendant fever, We conclude that signal-transducing mechanisms operating across the blood-brain barrier are most critical for the development of the febrile reponse to a systemic noxa.