ROLES OF INTERLEUKIN-1-BETA AND TUMOR-NECROSIS-FACTOR IN LIPOPOLYSACCHARIDE FEVER IN RATS
ROLES OF INTERLEUKIN-1-BETA AND TUMOR-NECROSIS-FACTOR IN LIPOPOLYSACCHARIDE FEVER IN RATS
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DOI：
10.1152/ajpregu.1990.259.4.r724
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发表时间：
1990-10-01
影响因子：
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通讯作者：
KLUGER, MJ
中科院分区：
文献类型：
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作者：
LONG, NC;OTTERNESS, I;KLUGER, MJ
白细胞介素 1.beta 的作用。 (IL-1.beta.)和肿瘤坏死因子-.alpha。在大鼠中研究了脂多糖（LPS）引起的发热中的（TNF）。我们使用针对 IL-1.beta 的抗血清。和 TNF 以确定我们是否可以通过阻断这些细胞因子的作用来改变发烧。静脉注射抗血清IL-1.β。腹腔注射 LPS 前 3.5 天，平均发热明显低于注射对照血清的大鼠（0.36±0.11 vs 0.82±0.16°C，P = 0.016）。腹腔注射LPS前3.5天静脉注射TNF抗血清并不能阻止发热，反而显着增强发热（1.31±0.16 vs. 0.82±0.16℃，P=0.027）。这些数据支持 IL-1.beta 的假设。 TNF 是 LPS 发热的重要原因，TNF 作为内源性解热剂，可限制大鼠 LPS 发热的程度。
The roles of interleukin 1.beta. (IL-1.beta.) and tumor necrosis factor-.alpha. (TNF) in lipopolysaccharide (LPS)-induced fever were investigated in the rat. We used antisera against IL-1.beta. and TNF to determine whether we could alter the fever by blocking the action of these cytokines. The intravenous injection of antiserum IL-1.beta. 3.5 days before the intraperitoneal injection of LPS resulted in a mean fever that was significantly lower than that seen in rats that had been injected with control serum (0.36 .+-. 0.11 vs 0.82 .+-. 0.16.degree.C, P = 0.016). The intravenous injection of antiserum against TNF 3.5 days before the intraperitoneal injection of LPS did not block the fever but significantly enhanced it (1.31 .+-. 0.16 vs. 0.82 .+-. 0.16.degree.C, P = 0.027). These data support the hypotheses that IL-1.beta. is responsible for a significant part of LPS fever and that TNF acts as an endogenous antipyretic to limit the magnitude of LPS fever in the rat.