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冷却和复温通过p38丝裂原活化蛋白激酶依赖性途径诱导人支气管上皮细胞中白细胞介素-8的表达。

Cooling and rewarming-induced IL-8 expression in human bronchial epithelial cells through p38 MAP kinase-dependent pathway.

作者信息

Gon Y, Hashimoto S, Matsumoto K, Nakayama T, Takeshita I, Horie T

机构信息

First Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.

出版信息

Biochem Biophys Res Commun. 1998 Aug 10;249(1):156-60. doi: 10.1006/bbrc.1998.9115.

DOI:10.1006/bbrc.1998.9115
PMID:9705848
Abstract

p38 mitogen-activated protein kinase (MAP) kinase is activated by various stresses; however, little is known about cold stress which has been shown to cause various inflammatory diseases. In the present study, we examined the effect of cold stimulation on interleukin-8 (IL-8) expression and a role of p38 MAP kinase in IL-8 expression in human bronchial epithelial cells (BEC) in order to clarify the mechanism in hypothermic temperature-induced inflammation. The results showed that cold stimulation induced tyrosine phosphorylation of p38 MAP kinase but not IL-8 expression. IL-8 expression in BEC was induce when the temperature of incubation changed from 1 degree C to 37 degrees C (cooling and rewarming). The specific p38 MAP kinase inhibitor SB 203580 inhibited cooling and rewarming-induced IL-8 expression, indicating that cooling and rewarming-induced IL-8 expression in BEC was mediated through p38 MAP kinase-dependent pathway.

摘要

p38丝裂原活化蛋白激酶(MAP激酶)可被多种应激激活;然而,对于已被证明会引发各种炎症性疾病的冷应激却知之甚少。在本研究中,我们检测了冷刺激对白细胞介素-8(IL-8)表达的影响以及p38 MAP激酶在人支气管上皮细胞(BEC)中IL-8表达中的作用,以阐明低温诱导炎症的机制。结果显示,冷刺激诱导了p38 MAP激酶的酪氨酸磷酸化,但未诱导IL-8表达。当孵育温度从1℃变为37℃(冷却和复温)时,BEC中的IL-8表达被诱导。特异性p38 MAP激酶抑制剂SB 203580抑制了冷却和复温诱导的IL-8表达,表明冷却和复温诱导的BEC中IL-8表达是通过p38 MAP激酶依赖性途径介导的。

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