Cytokines and chemokines in testicular inflammation:a brief review

GUAZZONE V.A.; JACOBO P.; THEAS M.S.; LUSTIG L.

MICROSCOPY RESEARCH AND TECHNIQUE.

WILEY-LISS, DIV JOHN WILEY & SONS INC

Año: 2009 vol. 72 p. 620 - 628

1059-910X

A wide spectrum of data in the literature shows the relevance of cytokines as paracrine regulators of spermatogenesis and steroidogenesis in the normal testis. In this brief review we highlight the relevance of cytokines in the testis, during inflammation. This phenomenon involves complex and multiple interactions among immune and germ cells generally resulting in the alteration of spermatogenesis. The complexity of these cell interactions is multiplied since Sertoli and Leydig cells are also producers of pro- and anti-inflammatory cytokines and chemokines. Also, cytokines are pleiotropic and they exert opposite and/or redundant effects in different conditions. However, in spite of this bidirectional immunoregulatory function of cytokines, the mass of the data, reported from experiments of acute testicular inflammation shows up-regulation of IL-1â, IL-1á, IL-6 and TNF-á which induce adverse effects on germ cells. In autoimmune orchitis, a chronic testicular inflammation, chemokines such as CCL2, CCL3 and CCL4 induce attraction and extravasation of immune cells within the testicular interstitium. These cells alter the normal immunosuppressor microenvironment principally through the secretion of pro-inflammatory cytokines, IFN-ã initially, and IL-6 and TNF-á thereafter. Germ cells expressing TNFR1, IL-6R and Fas increase in number and undergo apoptosis, through the TNF-á/TNFR1, IL-6/IL-6R and Fas/Fas L systems. The knowledge of immune-germ cell interactions in experimental models of testicular chronic inflammation will contribute to the understanding of the mechanisms by which chronic inflammatory conditions of the testis can disrupt the process of spermatogenesis.