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Endotoxin tolerance in rats: expression of TNF-alpha, IL-6, IL-10, VCAM-1 AND HSP 70 in lung and liver during endotoxin shock.

机译:大鼠内毒素耐受性:内毒素休克期间肺和肝中TNF-α,IL-6,IL-10,VCAM-1和HSP 70的表达。

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摘要

Endotoxin can induce a state of tolerance against its own pathological effects, commonly referred to as endotoxin tolerance. This phenomenon has been found to be associated with reduced serum levels of cytokines such as TNF-alpha, IL-1, IL-6 and IL-10. In the present study the expression of TNF-alpha, IL-6, IL-10, the adhesion molecule VCAM-1 and the heat shock protein 70 was determined in vivo in lung and liver of LPS-tolerant and naive rats by means of semiquantitative RT-PCR after i.v. LPS injection. TNFalpha, IL-6, IL-10, HSP 70 and VCAM-1 were induced in lung and liver after LPS injection. In liver and lung of endotoxin-tolerant rats TNF-alpha and IL-6 were induced to a lower degree after LPS treatment when compared to non-tolerant controls. The LPS-induced IL-10 expression was also slightly attenuated in the lung of tolerant rats, but in the liver no differences between tolerant and non-tolerant animals were observed. HSP 70 and VCAM-1 were expressed after systemic LPS treatment in liver and lung. The degree of induction, however, was the same in tolerant and untreated controls. The presented data show that endotoxin tolerance is reflected by a reduced cytokine expression in lung and liver in vivo. On the other hand, levels of expression of the adhesion molecule VCAM-1 and the stress protein HSP 70 do not appear to be changed by endotoxin tolerance. Copyright 1999 Academic Press.
机译:内毒素可以诱导对自身病理作用的耐受状态,通常称为内毒素耐受。已经发现这种现象与血清细胞因子如TNF-α,IL-1,IL-6和IL-10的降低有关。在本研究中,通过半定量法测定了耐LPS和天真大鼠肺和肝脏中TNF-α,IL-6,IL-10,黏附分子VCAM-1和热休克蛋白70的表达。静脉内RT-PCR LPS注射。注射LPS后在肺和肝中诱导TNFalpha,IL-6,IL-10,HSP 70和VCAM-1。与非耐受性对照相比,在接受内毒素耐受的大鼠的肝和肺中,LPS处理后,TNF-α和IL-6的诱导程度较低。在耐受性大鼠的肺中,LPS诱导的IL-10表达也略有减弱,但是在肝脏中,未观察到耐受性和非耐受性动物之间的差异。全身LPS治疗后,HSP 70和VCAM-1在肝和肺中表达。然而,诱导程度在耐受和未治疗对照中相同。所提供的数据表明内毒素耐受性通过体内肺和肝中细胞因子表达的减少反映出来。另一方面,粘附分子VCAM-1和应激蛋白HSP 70的表达水平似乎没有因内毒素耐受而改变。版权所有1999,学术出版社。

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