Effect of homologous interleukin-1, interleukin-6 and tumor necrosis factor-alpha on the core body temperature of mice.
Effect of homologous interleukin-1, interleukin-6 and tumor necrosis factor-alpha on the core body temperature of mice.
复制标题
同源白细胞介素1、白细胞介素6和肿瘤坏死因子-α对小鼠核心体温的影响。
DOI：
10.1159/000097341
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发表时间：
1997
影响因子：
2.4
通讯作者：
Dunn,AJ
中科院分区：
文献类型：
--
作者：
Wang,J;Ando,T;Dunn,AJ
使用放置在腹腔中的电池供电的遥测装置测试脂多糖（LPS）和同源细胞因子对小鼠核心温度的影响。腹腔注射1 μ g LPS对核心体温（Tc）产生双相作用，Tc迅速下降，在30-45分钟左右达到峰值，然后在150-300分钟左右持续上升。当使用更高剂量的LPS（5 μ g）时，低温程度增加，持续时间更长，并且没有观察到发烧。用吲哚美辛（一种环氧合酶抑制剂）预处理小鼠，可防止LPS引起的Tc降低和升高，但一氧化氮合酶抑制剂不能。小鼠白细胞介素-1 β（mIL-1β，100 ng，ip）诱导的变化与LPS相似，即Tc短暂降低，随后小幅升高。当注射1 μg mIL-1β时，观察到持续超过3 h的深度低温。小鼠IL-6（1 μg）静脉（iv）或ip给药后不能改变核心温度。人IL-6也无效。重组小鼠肿瘤坏死因子-α（mTNFα）1 μg（ip或iv）也不能改变小鼠的核心温度。然而，较高剂量的mTNFα（5 μg ip）导致Tc短暂降低，随后小幅升高。LPS和细胞因子在C57 B1/6 J小鼠中获得了类似的结果，除了mIL-1β在该品系中无效。这些结果表明，对IL-1、IL-6和TNFα给药的内分泌、神经化学和行为反应不能用Tc的变化来解释，尽管它们可能有助于这些反应。他们还表明，IL-1β可能解释了LPS后观察到的发热，但这些细胞因子可能不是LPS诱导的Tc变化的唯一因素。版权所有© 1997 S. Karger AG，巴塞尔
Lipopolysaccharide (LPS) and homologous cytokines were tested for their effect on core temperature in mice using battery-operated telemetric devices placed in the peritoneal cavity. One microgram LPS injected intraperitoneally (ip) induced a biphasic effect on core body temperature (Tc), a rapid decrease in Tcwith a peak around 30-45 min followed by a prolonged rise around 150-300 min. When a higher dose of LPS (5 jxg) was used, the hypothermia was increased in magnitude and lasted much longer, and no fever was observed. Both the decrease and the increase in Tccaused by LPS were prevented by pretreating the mice with indomethacin, a cyclooxygenase inhibitor, but not by a nitric oxide synthase inhibitor. Mouse interleukin-1β (mIL-1β, 100 ng, ip) induced changes resembling those to LPS, a short-lived decrease in Tc, followed by a small increase. When 1 μg mIL-1β was injected a profound hypothermia lasting more than 3 h was observed. Mouse IL-6 (1 μg) failed to alter core temperature after either intravenous (iv) or ip administration. Human IL-6 was also ineffective. Recombinant mouse tumor necrosis factor-α (mTNFα) also failed to alter the core temperature of mice when injected at a dose of 1 μg (ip or iv). However, a higher dose of mTNFα (5 μg ip) caused a short-lived decrease in Tc, followed by a small increase. Similar results were obtained with LPS and the cytokines in C57B1/6J mice, except that mIL-1β was ineffective in this strain. These results indicate that the endocrine, neurochemical and behavioral responses to IL-1, IL-6 and TNFα administration cannot be explained by changes in Tc, although they may contribute to them. They also suggest that IL-1β may account for the fever observed following LPS, but that these cytokines are probably not the only factors involved in LPS-induced changes in Tc. Copyright© 1997 S. Karger AG, Basel