详细信息
Innate immune responses of epididymal epithelial cells to Staphylococcus aureus infection ( SCI-EXPANDED收录) 被引量:33
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, Yun-Tao[1,2];Guo, Jing-Hui[1];Wu, Zhong-Luan[1];Xiong, Yuan[1];Zhou, Wen-Liang[1]
机构:[1]Sun Yat Sen Univ, Sch Life Sci, Guangzhou 510275, Guangdong, Peoples R China;[2]Guangdong Ocean Univ, Modern Biochem Ctr, Zhanjiang 524088, Peoples R 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:SCI-EXPANDED(收录号:WOS:000258480400014)、、WOS
语种:英文
外文关键词:epididymal epithelial cells; Staphylococcus aureus; Toll-like receptors; innate immune responses; p38 MAPK; NF-kappa B
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-alpha and IL-1 beta 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-kappa B 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-kappa B 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-kappa B after TLR2 activation by S. aureus infection. (C) 2008 Elsevier B.V. All rights reserved.
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