Prior stressor exposure sensitizes LPS-induced cytokine production
Prior stressor exposure sensitizes LPS-induced cytokine production
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DOI：
10.1006/brbi.2001.0638
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发表时间：
2002-08-01
影响因子：
15.1
通讯作者：
Maier, SF
中科院分区：
文献类型：
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作者：
Johnson, JD;O'Connor, KA;Maier, SF
暴露于压力源通常会改变许多系统的后续反应。本研究测试了先前暴露于不可避免的尾震（IS）是否会改变白细胞介素(IL)-1 β、肿瘤坏死因子(TNF)- α或IL-6对注射细菌内毒素（脂多糖LPS）的反应，暴露于IS的大鼠或仍作为家笼对照（HCC）；24 h后，动物腹腔注射10杯/千克LPS或等量无菌生理盐水。与对照组相比，IS显著增加LPS后1小时血浆tnf - α、il -1 β和垂体、下丘脑、海马、小脑il -1 β，但不增加2小时。在暴露于IS后4、10或21天注射LPS或生理盐水，收集尾静脉血液并检测il -1 β。血浆il -1 β反应在IS后4天出现增强，但10天后消失。这些结果表明，暴露于IS通过导致促炎细胞因子的更大或更快的诱导，使先天免疫反应对LPS增敏。(C) 2001 Elsevier Science（美国）
Exposure to stressors often alters the subsequent responsiveness of many systems. The present study tested whether prior exposure to inescapable tailshock (IS) alters the interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, or IL-6 response to an injection of bacterial endotoxin (lipopolysaccharide LPS), Rats were exposed to IS or remained as home cage controls (HCC); 24 h later animals were injected i.p. with either 10 mug/kg LPS or equilvolume sterile saline. IS significantly increased plasma TNF-alpha, IL-1beta, and pituitary, hypothalamus, hippocampus, cerebellum IL-1beta 1 h, but not 2 h, after LPS, compared to controls. Additional animals were injected with LPS or saline 4, 10, or 21 days after exposure to IS and tail vein blood was collected and assayed for IL-1beta. An enhanced plasma IL-1beta response occurred 4 days after IS, but was gone by 10 days. These results suggest that exposure to IS sensitizes the innate immune response to LPS by resulting in either a larger or a more rapid induction of proinflammatory cytokines. (C) 2001 Elsevier Science (USA).