Recombinant tumor necrosis factor and interleukin 1 enhance slow-wave sleep.
Recombinant tumor necrosis factor and interleukin 1 enhance slow-wave sleep.
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DOI：
10.1152/ajpregu.1987.253.1.r142
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发表时间：
1987-07
期刊：
影响因子：
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通讯作者：
S. Shoham;D. Davenne;A. Cady;C. Dinarello;J. Krueger
中科院分区：
文献类型：
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作者：
S. Shoham;D. Davenne;A. Cady;C. Dinarello;J. Krueger
细胞因子白细胞介素1（IL 1）和干扰素（IFN）是免疫应答调节剂，也是致热性和致眠性的。肿瘤坏死因子（TNF）（恶病质）是另一种热原性单核细胞产物，其产生可由致眠剂如内毒素引起。因此，测定了人重组TNF（rTNF）的致眠活性。静脉（iv）或脑室内（ICV）注射rTNF可增强慢波睡眠（SWS）和脑电图慢波（0.5-4.0 Hz）活动。重组TNF还抑制快速眼动睡眠（REM），并诱导双相发热，无论是静脉注射或ICV注射。将对rTNF的反应与人重组β-IL 1（rIL 1）引起的反应进行比较。rIL 1引起的睡眠反应与先前报道的天然IL 1和rTNF引起的睡眠反应相似。然而，与rTNF不同，rIL 1诱导迟发性发热。动物的行为和脑温度的变化，发生在从一个觉醒状态到另一个保持不受干扰后，无论是rTNF或rIL 1治疗。TNF和IL 1以及其他免疫活性物质，IFN、胞壁肽和内毒素增强SWS，表明SWS与免疫应答有关。我们的结论是，除了IL 1和IFN之外，TNF也是一种内源性睡眠原。
The cytokines interleukin 1 (IL 1) and interferon (IFN) are immune response modifiers that are also pyrogenic and somnogenic. Tumor necrosis factor (TNF) (cachectin) is another pyrogenic monocyte product whose production can be elicited by somnogenic agents such as endotoxin. Human recombinant TNF (rTNF), therefore, was assayed for somnogenic activity. Intravenous (iv) or intracerebroventricular (ICV) injections of rTNF enhanced slow-wave sleep (SWS) and electroencephalographic slow-wave (0.5-4.0 Hz) activity. Recombinant TNF also suppressed rapid-eye-movement sleep (REM) and induced biphasic fevers whether given by intravenous or ICV injection. Responses to rTNF were compared with those elicited by human recombinant beta-IL 1 (rIL 1). Sleep responses elicited by rIL 1 were similar to those previously reported for native IL 1 and to those elicited by rTNF. However, unlike rTNF, rIL 1 induced monophasic fevers. Animal behavior and brain temperature changes that occur during the transition from one arousal state to another remained undisturbed after either rTNF or rIL 1 treatment. The fact that TNF and IL 1 as well as other immunoactive substances, e.g., IFN, muramyl peptides, and endotoxin, enhance SWS suggests that SWS is linked to the immune response. We conclude that TNF, in addition to IL 1 and IFN, is an endogenous somnogen.