文献类型：期刊文献

英文题名：Innate immune responses of epididymal epithelial cells to Staphylococcus aureus infection

作者：Zhao Y.-T.; Guo J.-H.; Wu Z.-L.; Xiong Y.; Zhou W.-L.

机构：[1]School of Life Science, Sun Yat-Sen University, Guangzhou, 510275, 135 Xin-gang West Road, China;[2]Modern Biochemistry Center, Guangdong Ocean University, Zhanjiang, 524088, China

年份：2008

卷号：119

期号：1-2

起止页码：84

外文期刊名：Immunology Letters

收录：Scopus(收录号：2-s2.0-47149117948)

语种：英文

外文关键词：Epididymal epithelial cells; Innate immune responses; NF-κB; p38 MAPK; Staphylococcus aureus; Toll-like receptors

外文摘要：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-α and IL-1β 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-κB inhibitor BAY11-7082 inhibited TNF-α secretion completely and p38 mitogen-activated protein kinases (MAPKs) inhibitor SB203580 decreased TNF-α secretion partly, indicating that NF-κB 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-κB after TLR2 activation by S. aureus infection. ? 2008 Elsevier B.V. All rights reserved.