title: Expression and regulation of the CC-chemokine monocyte chemoattractant protein-1 in rat testicular cells in primary culture.
abstract: Testicular inflammation is classically observed in pathogenesis caused by infectious agents, environmental toxins, trauma, or autoimmune reactions and can lead to transitory or even permanent sterility. In these situations, a leukocyte infiltration is generally encountered. Macrophage inflammatory proteins (MIP)-1alpha and -1beta and monocyte chemoattractant protein-1 (MCP-1) are CC-chemokines involved in macrophage and lymphocyte chemoattraction. In the present study, using reverse transcription-polymerase chain reaction, Northern blot, and a specific ELISA, we investigated whether or not these chemokines are present within the testis and whether they are induced by a number of proinflammatory cytokines and lipopolysaccharides (LPS). MIP-1alpha and MIP-1beta were not detected in Sertoli cells, germ cells, peritubular cells, or Leydig cells. In contrast, MCP-1 mRNA and protein were found to be expressed by control isolated peritubular cells, and expression was markedly stimulated by interleukin-1alpha and-1beta (IL-1alpha and IL-1beta), tumor necrosis factor alpha (TNF-alpha), interferon gamma, and LPS. Leydig cells expressed MCP-1 when stimulated by IL-1beta. In contrast, MCP-1 was not found to be produced by Sertoli cells or germ cells as established by Northern blot and ELISA techniques. The kinetics of MCP-1 production by peritubular cells, as demonstrated by expression as early as 8 h poststimulation, are compatible with there being a rapid mobilization of these cells and this chemokine in an inflammatory process. Moreover, MCP-1 production by peritubular cells after half-maximal stimulation by LPS, TNF-alpha, and IL-1beta (2 pg/ml-0.9 ng/ml) is also compatible with the physiologic concentrations of the proinflammatory cytokines generally found in an inflammatory site. It is concluded that MCP-1 is produced by Leydig cells and peritubular cells and that it could be involved in the mobilization and migration of leukocytes observed during testicular inflammation.
authors.affiliation: GERM-INSERM U. 435, Université de Rennes I, Campus de Beaulieu, 35042 Rennes cedex, Bretagne, France.
authors.forename: F
authors.initials: F
authors.lastname: Aubry
authors.forename: C
authors.initials: C
authors.lastname: Habasque
authors.forename: A P
authors.initials: AP
authors.lastname: Satie
authors.forename: B
authors.initials: B
authors.lastname: Jégou
authors.forename: M
authors.initials: M
authors.lastname: Samson
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics* / Q000378:metabolism*; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D005786:Gene Expression Regulation; D007375:Interleukin-1 / Q000494:pharmacology; D007985:Leydig Cells / Q000502:physiology; D008070:Lipopolysaccharides / Q000494:pharmacology; D019402:Macrophage Inflammatory Proteins / Q000235:genetics* / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012708:Sertoli Cells / Q000502:physiology; D013094:Spermatozoa / Q000502:physiology; D013737:Testis / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D007375:Interleukin-1; D008070:Lipopolysaccharides; D019402:Macrophage Inflammatory Proteins; D014409:Tumor Necrosis Factor-alpha