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内源性白细胞介素-10在急性炎症模型中对巨噬细胞炎性蛋白-1α表达和功能的调节

Regulation of macrophage inflammatory protein-1 alpha expression and function by endogenous interleukin-10 in a model of acute inflammation.

作者信息

Ajuebor M N, Das A M, Virág L, Szabó C, Perretti M

机构信息

Department of Biochemical Pharmacology, The William Harvey Research Institute, London, United Kingdom.

出版信息

Biochem Biophys Res Commun. 1999 Feb 16;255(2):279-82. doi: 10.1006/bbrc.1999.0196.

DOI:10.1006/bbrc.1999.0196
PMID:10049699
Abstract

In this study we have determined the role of endogenous interleukin (IL)-10 on leucocyte recruitment and production of the CC chemokine macrophage inflammatory protein-1alpha (MIP-1alpha) in a murine model of acute inflammation. Intraperitoneal injection of zymosan produced a dose-dependent cellular infiltration which was concomitant with MIP-1alpha release in the lavage fluids. Release of this chemokine had a functional role since treatment of mice with a specific anti-MIP-1alpha antibody reduced both neutrophil and monocyte accumulation into the peritoneal cavity. An unexpected increase in cell influx and MIP-1alpha production was measured following depletion of resident peritoneal macrophages, as achieved by a 3-day liposome treatment. A similar result was obtained when the zymosan peritonitis response was elicited in IL-10 knock-out mice. In summary we propose a functional cross talk between endogenous IL-10 and this CC chemokine during the host inflammatory response.

摘要

在本研究中,我们在急性炎症小鼠模型中确定了内源性白细胞介素(IL)-10对白细胞募集以及CC趋化因子巨噬细胞炎性蛋白-1α(MIP-1α)产生的作用。腹腔注射酵母聚糖可产生剂量依赖性细胞浸润,这与灌洗液中MIP-1α的释放同时发生。这种趋化因子的释放具有功能性作用,因为用特异性抗MIP-1α抗体处理小鼠可减少中性粒细胞和单核细胞向腹腔的积聚。通过3天脂质体处理耗尽腹腔常驻巨噬细胞后,测量到细胞流入和MIP-1α产生意外增加。在IL-10基因敲除小鼠中引发酵母聚糖腹膜炎反应时也获得了类似结果。总之,我们提出在宿主炎症反应期间内源性IL-10与这种CC趋化因子之间存在功能性相互作用。

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