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Production of the Chemokines Monocyte Chemotactic Protein-1, Regulated on Activation Normal T Cell Expressed and Secreted Protein, Growth-Related Oncogene, and Interferon--Inducible Protein-10 Is Induced by the Sendai Virus in Human and Rat Testicular Cells

GERM-INSERM, U-435, Université de Rennes I, Campus de Beaulieu (R.L.G., T.M., F.A., B.J., M.S.), 35042 Rennes, Bretagne, France; Service d’Urologie, CHU Ponchaillou (J.-J.P.), 35000 Rennes, Bretagne, France; and Service de Bactériologie-Virologie, CHU Ponchaillou (A.R.), 35000 Rennes, Bretagne, France

Address all correspondence and requests for reprints to: Dr. Michel Samson, Université de Rennes I, GERM-INSERM, U-435, Campus de Beaulieu, 35042 Rennes Cedex, Bretagne, France. E-mail: .

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-, and interferon--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-, and interferon--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.

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