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仙台病毒可诱导人及大鼠睾丸细胞产生趋化因子单核细胞趋化蛋白-1、激活正常T细胞表达和分泌的调节蛋白、生长相关癌基因及γ干扰素诱导蛋白-10。

Production of the chemokines monocyte chemotactic protein-1, regulated on activation normal T cell expressed and secreted protein, growth-related oncogene, and interferon-gamma-inducible protein-10 is induced by the Sendai virus in human and rat testicular cells.

作者信息

Le Goffic Ronan, Mouchel Thomas, Aubry Florence, Patard Jean-Jacques, Ruffault Annick, Jégou Bernard, Samson Michel

机构信息

GERM-INSERM, U-435, Université de Rennes I, Campus de Beaulieu, 35042 Rennes, Bretagne, France.

出版信息

Endocrinology. 2002 Apr;143(4):1434-40. doi: 10.1210/endo.143.4.8735.

DOI:10.1210/endo.143.4.8735
PMID:11897701
Abstract

Several viruses infect the testis, inducing inflammation, which may lead to infertility. In this study we investigated the production in rat and human testicular cells exposed to the Sendai virus of several chemokines that play a major role in inflammatory processes. Exposure of rat testicular macrophages and Sertoli, Leydig, and peritubular cells to the Sendai virus led to the production of mRNA and protein for monocyte chemotactic protein-1 (MCP-1), regulated on activation normal T cell expressed and secreted protein, growth-related oncogene-alpha, and interferon-gamma-inducible protein-10. In rat peritubular cells exposed to the Sendai virus, MCP-1 production was time and dose dependent. In contrast, rat germ cells did not produce these chemokines. Chemokine synthesis was detected in human Leydig cells exposed to the Sendai virus, but not in human total germ cells, suggesting that rats and humans display similar responses in terms of chemokine production. MCP-1, regulated on activation normal T cell expressed and secreted protein, growth-related oncogene-alpha, and interferon-gamma-inducible protein-10 have been reported to be chemoattractants for a large variety of leukocytes. The ability of the Sendai virus to induce chemokine production in somatic cells (mostly peritubular and Leydig cells) may therefore increase the recruitment of leukocytes to sites of infection.

摘要

几种病毒可感染睾丸,引发炎症,进而可能导致不育。在本研究中,我们调查了暴露于仙台病毒的大鼠和人类睾丸细胞中几种在炎症过程中起主要作用的趋化因子的产生情况。将大鼠睾丸巨噬细胞、支持细胞、间质细胞和睾丸周细胞暴露于仙台病毒,会导致单核细胞趋化蛋白-1(MCP-1)、活化正常T细胞表达和分泌的调节蛋白、生长相关癌基因-α以及干扰素-γ诱导蛋白-10的mRNA和蛋白质的产生。在暴露于仙台病毒的大鼠睾丸周细胞中,MCP-1的产生呈时间和剂量依赖性。相比之下,大鼠生殖细胞不产生这些趋化因子。在暴露于仙台病毒的人类间质细胞中检测到趋化因子合成,但在人类总生殖细胞中未检测到,这表明大鼠和人类在趋化因子产生方面表现出相似的反应。据报道,MCP-1、活化正常T细胞表达和分泌的调节蛋白、生长相关癌基因-α以及干扰素-γ诱导蛋白-10是多种白细胞的趋化剂。因此,仙台病毒在体细胞(主要是睾丸周细胞和间质细胞)中诱导趋化因子产生的能力可能会增加白细胞向感染部位的募集。

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