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嗜酸乳杆菌NCFM的表层蛋白抑制肠道病原体诱导的HT-29细胞凋亡。

Surface layer protein from Lactobacillus acidophilus NCFM inhibit intestinal pathogen-induced apoptosis in HT-29 cells.

作者信息

Meng Jun, Zhang Qiu-Xiang, Lu Rong-Rong

机构信息

School of Food Science and Technology, Henan University of Technology, Zhengzhou, Henan Province 450001, China; State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu 214122, China.

State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu 214122, China.

出版信息

Int J Biol Macromol. 2017 Mar;96:766-774. doi: 10.1016/j.ijbiomac.2016.12.085. Epub 2017 Jan 3.

DOI:10.1016/j.ijbiomac.2016.12.085
PMID:28057572
Abstract

Intestinal pathogens have been proposed to adhere to epithelial cells and cause apoptosis. This study was to investigate the inhibitory effects of surface layer protein (SLP, 46kDa) from Lactobacillus acidophilus NCFM on Escherichia coli and Salmonella-induced apoptosis in HT-29 cells and the mechanism of the inhibition was also studied. The SLP could alleviate the chromatin condensation caused by intestinal pathogens as observed under fluorescent microscope. Flow cytometry analysis showed that the SLP decreased E. coli and Salmonella-induced apoptosis by 46% and 48%, respectively. The SLP could also inhibit the mitochondrial membrane potential reduction and Ca level increase in HT-29 cells. Furthermore, the activation of caspase-9 and caspase-3 induced by E. coli and Salmonella was significantly decreased by the addition of SLP. These results suggested that L. acidophilus NCFM SLP could protect HT-29 cells against intestinal pathogen-induced apoptosis through a mitochondria-mediated pathway. These findings may reveal a new method for the treatment of intestinal infection and provide a theoretical basis for the practical application of SLP in food, biological and pharmaceutical fields.

摘要

肠道病原体被认为可黏附于上皮细胞并导致细胞凋亡。本研究旨在探讨嗜酸乳杆菌NCFM的表层蛋白(SLP,46kDa)对大肠杆菌和沙门氏菌诱导HT-29细胞凋亡的抑制作用,并研究其抑制机制。荧光显微镜观察发现,SLP可减轻肠道病原体引起的染色质凝聚。流式细胞术分析表明,SLP分别使大肠杆菌和沙门氏菌诱导的细胞凋亡减少了46%和48%。SLP还可抑制HT-29细胞线粒体膜电位降低和钙水平升高。此外,添加SLP可显著降低大肠杆菌和沙门氏菌诱导的caspase-9和caspase-3的激活。这些结果表明,嗜酸乳杆菌NCFM SLP可通过线粒体介导的途径保护HT-29细胞免受肠道病原体诱导的凋亡。这些发现可能揭示一种治疗肠道感染的新方法,并为SLP在食品、生物和制药领域的实际应用提供理论依据。

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