bay-11-7082 and Genital-Diseases--Male

The epithelium is an active participant in the host response to infection. We hypothesized that epididymal epithelia play a role in the innate immune responses by sensing the presence of pathogens, expressing and secreting inflammatory cytokines that recruit inflammatory cells in response to invading pathogens. Our results indicated that TNF-alpha and IL-1beta could be secreted by the primary cultured rat epididymal cauda epithelia infected with Staphylococcus aureus. Epididymal epithelial-induced nitric oxide synthase (iNOS) expression was up-regulated after S. aureus infection and nitric oxide (NO) was also found to be produced significantly. NF-kappaB inhibitor BAY11-7082 inhibited TNF-alpha secretion completely and p38 mitogen-activated protein kinases (MAPKs) inhibitor SB203580 decreased TNF-alpha secretion partly, indicating that NF-kappaB and p38 signal pathways were involved in this inflammation response. Toll-like receptor (TLR)-2 and -4 were shown to be expressed in primary cultured rat epididymal epithelia. After infection the level of TLR2 expression was up-regulated rather than TLR4. These results demonstrated that epididymal epithelium have an innate immune response through activation of p38 MAPK and NF-kappaB after TLR2 activation by S. aureus infection.

Topics: Animals; Cell Culture Techniques; Epididymis; Epithelial Cells; Gene Expression Regulation; Genital Diseases, Male; Imidazoles; Immunity, Innate; Interleukin-1beta; Intracellular Signaling Peptides and Proteins; Male; NF-kappa B; Nitric Oxide; Nitric Oxide Synthase Type II; Nitriles; Protein Serine-Threonine Kinases; Pyridines; Rats; Rats, Sprague-Dawley; Signal Transduction; Staphylococcal Infections; Staphylococcus aureus; Sulfones; Tumor Necrosis Factor-alpha