Central injection of interleukin-13 potentiates LPS-induced sickness behavior in rats
Central injection of interleukin-13 potentiates LPS-induced sickness behavior in rats
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DOI：
10.1097/00001756-200112210-00025
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发表时间：
2001-12-21
期刊：
影响因子：
1.7
通讯作者：
Dantzer, R
中科院分区：
文献类型：
--
作者：
Bluthé, RM;Bristow, A;Dantzer, R
细菌内毒素脂多糖（LPS）的全身给药对行为具有深刻的抑制作用，所述抑制作用是由脑中促炎细胞因子如白细胞介素-1（IL-1）、IL-6和肿瘤坏死因子-α（TNF-α）的诱导性表达介导的。为了评估抗炎细胞因子IL-13对LPS诱导的疾病行为的调节作用，将腹腔注射LPS的大鼠i. c. v.给予大鼠重组IL-13。当两种分子共注射时，IL-13（300 ng）增强LPS（125 μ g/kg）的行为作用。在LIPS（150 μ g/kg）之前12小时给予IL-13（300 ng）并不能阻断LPS对社会探索的抑制作用。这些结果表明IL-13在脑中充当促炎细胞因子。NeuroReport 12：3979-3983（C）2001 Lippincott威廉姆斯和威尔金斯。
Systemic administration of the bacterial endotoxin lipopolysaccharide (LPS) has profound depressive effects on behavior that are mediated by the inducible expression of proinflammatory cytokines such as interleukin-1 (IL-1), IL-6 and tumor necrosis factor-alpha (TNF-alpha) in the brain. To assess the regulatory effects of the anti-inflammatory cytokine IL-13 on LPS-induced sickness behavior, rats injected i.p. with LPS were administered rat recombinant IL-13 i.c.v. IL-13 (300 ng) potentiated the behavioral effects of LPS (125 mug/kg) when both molecules were coinjected. Administration of IL-13 (300 ng) 12 h prior to LIPS (150 mug/kg) did not block the depressing effects of LPS on social exploration. These results indicate that IL-13 acts as a proinflammatory cytokine in the brain. NeuroReport 12:3979-3983 (C) 2001 Lippincott Williams & Wilkins.