Antiserum against tumor necrosis factor increases stress hyperthermia in rats.

Antiserum against tumor necrosis factor increases stress hyperthermia in rats.
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抗肿瘤坏死因子的抗血清会增加大鼠的应激性高热。

DOI:
10.1152/ajpregu.1990.258.3.r591
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发表时间:
1990
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Kluger,MJ
Kluger,MJ
中科院分区:
--
文献类型:
--
作者:
Long,NC;Vander,AJ;Kunkel,SL;Kluger,MJ

文献摘要

被引文献

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心理压力(例如,暴露在一个新的环境中)会使老鼠的体温迅速升高。在这项研究中,我们研究了身体活动和免疫细胞因子肿瘤坏死因子或肿瘤坏死素(TNF)在这种温度变化中的作用。白天换笼应激大鼠体温升高与活动增加相关性较差(r = 0.07; P = 0.84),夜间换笼应激大鼠体温升高与活动增加呈负相关(r = 0.64; P = 0.04)。暴露于野外应激后的大鼠血浆和脑脊液中未检测到TNF。然而,在暴露于野外应激前3.5小时注射抗TNF血清导致的高热明显高于对照组注射血清的大鼠(1.38 +/- 0.11 vs. 0.79 +/- 0.14℃;P = 0.002)。注射抗tnf的大鼠在换笼应激后的峰值温度变化也同样增加(0.82 +/- 0.08 vs 0.50 +/- 0.08℃;P = 0.016)。这种增强的高热与注射抗肿瘤坏死因子血清的动物在脂多糖热后期出现的高热相似。这些数据支持以下假设:应激性热疗是一种真正的发热,TNF是一种内源性解热药,限制了这种发热的程度。
Psychological stress (e.g., exposure to a novel environment) causes a rapid rise in body temperature in rats. In this study, we examined the roles of physical activity and the immune cytokine tumor necrosis factor or cachectin (TNF) in this temperature change. The elevation in temperature of rats exposed to cage-switch stress during the day correlated poorly with the increase in activity (r = 0.07; P = 0.84) and, during cage switch at night, correlated negatively (r = 0.64; P = 0.04). TNF was not detected in the plasma or cerebrospinal fluid of rats after exposure to open-field stress. However, the injection of antiserum against TNF 3.5 h before exposure to the stress of being in an open field resulted in a significantly greater hyperthermia than was seen in the control serum-injected rats (1.38 +/- 0.11 vs. 0.79 +/- 0.14 degrees C; P = 0.002). The peak temperature change after cage-switch stress was similarly increased in rats that had been injected with anti-TNF (0.82 +/- 0.08 vs. 0.50 +/- 0.08 degrees C; P = 0.016). This enhanced hyperthermia is similar to the excessively high fever that occurs during the later phase of lipopolysaccharide fever in animals that have been injected with antiserum against TNF. These data support the hypotheses that stress hyperthermia is a true fever and that TNF is an endogenous antipyretic, limiting the magnitude of this fever.