Expression and regulation of the CC-chemokine monocyte chemoattractant protein-1 in rat testicular cells in primary culture

Biol Reprod. 2000 May;62(5):1427-35. doi: 10.1095/biolreprod62.5.1427.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Northern
  • Cells, Cultured
  • Chemokine CCL2 / genetics*
  • Chemokine CCL2 / metabolism*
  • Chemokine CCL3
  • Chemokine CCL4
  • Gene Expression Regulation
  • Interleukin-1 / pharmacology
  • Leydig Cells / physiology
  • Lipopolysaccharides / pharmacology
  • Macrophage Inflammatory Proteins / genetics*
  • Macrophage Inflammatory Proteins / metabolism*
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Sertoli Cells / physiology
  • Spermatozoa / physiology
  • Testis / cytology
  • Testis / drug effects
  • Testis / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Chemokine CCL2
  • Chemokine CCL3
  • Chemokine CCL4
  • Interleukin-1
  • Lipopolysaccharides
  • Macrophage Inflammatory Proteins
  • Tumor Necrosis Factor-alpha