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* Department of Histology and Medical Embryology, Istituto Pasteur-Fondazione Cenci Bolognetti, University of Rome "La Sapienza," Rome, Italy;
Department of Experimental Medicine, University of L’Aquila, L’Aquila, Italy; and
Department of Surgery "Pietro Valdoni," University of Rome "La Sapienza," Rome, Italy
TLRs play a crucial role in early host defense against invading pathogens. In the seminiferous epithelium, Sertoli cells are the somatic nurse cells that mechanically segregate germ cell autoantigens by means of the blood-tubular barrier and create a microenvironment that protects germ cells from both interstitial and ascending invading pathogens. The objective of this study was to examine TLR expression and their functional responses to specific agonists in mouse Sertoli cells. We measured the expression of TLR2, TLR4, TLR5, and TLR6 mRNAs and confirmed by FACS analysis the presence of proteins TLR2 and TLR5 on which we focused our study. Stimulation of Sertoli cells with macrophage-activating lipopeptide-2, agonist of TLR2/TLR6, and with flagellin, agonist of TLR5, induces augmented secretion of the chemokine MCP-1. To assess the functional significance of MCP-1 production following TLR stimulation, conditioned medium from either macrophage-activating lipopeptide-2 or flagellin-treated Sertoli cells was tested for in vitro chemotaxis assay, and a significant increase of macrophage migration was observed in comparison with unstimulated conditioned medium. Moreover, we studied the role of NF-
B and of MAPKs in regulating TLR-mediated MCP-1 secretion by using inhibitors specific for each transduction pathway and we demonstrated a pivotal role of the IB/NF-B and JNK systems. In addition, TLR2/TLR6 and TLR5 stimulation induces increased ICAM-1 expression in Sertoli cells. Collectively, this study demonstrates the novel ability of Sertoli cells to potentially respond to a wide variety of bacteria through TLR stimulation.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by grants from Ministero dell’Università e della Ricerca Scientifica e Tecnologica COFIN 2005.
2 A.R. and D.S. contributed equally to this work.
3 Address correspondence and reprint requests to Dr. Anna Riccioli, Department of Histology and Medical Embryology, University of Rome "La Sapienza," 00161 Rome, Italy. E-mail address: anna.riccioli{at}uniroma1.it
4 Abbreviations used in this paper: PSMC, peritubular smooth muscle cell; TIR, TLR/IL-1; SCCM, Sertoli cell conditioned medium; β-gal, β-galactosidase; CTR, untreated; MALP-2, macrophage-activating lipopeptide-2.
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