Lactobacillus plantarum ameliorates tumour necrosis factor-induced bacterial translocation in Caco-2 cells by regulation of TLR4 expression
Lactobacillus plantarum ameliorates tumour necrosis factor-induced bacterial translocation in Caco-2 cells by regulation of TLR4 expression
复制标题
DOI：
10.1099/jmm.0.000762
复制
发表时间：
2018-07-01
影响因子：
3
通讯作者：
Chen, Jun
中科院分区：
文献类型：
--
作者：
Wang, Bin;Li, Jingjing;Chen, Jun
目的。细菌跨肠屏障的易位在全身性败血症的发病机制中是重要的。在炎症条件下，共生菌以tlr4依赖的方式利用胞吞途径穿过肠上皮。本研究的目的是验证植物乳杆菌通过调节toll样受体-4表达来改善肿瘤坏死因子诱导的细菌易位的假设。研究了L. plantarum菌株抑制大肠杆菌B5对Caco-2细胞初始粘附的能力。研究了植物乳杆菌对tnf - α诱导的大肠杆菌B5跨Caco-2细胞易位的抑制作用。同时通过上皮电阻、HRP通透性、LDH释放和紧密连接蛋白的分布来评估屏障功能和完整性。RT-PCR检测TLR4的表达。结果/重要发现。用植物乳杆菌L2预处理单层膜可显著降低大肠杆菌B5的粘附和细胞内化(P
Purpose. Translocation of bacteria across the intestinal barrier is important in the pathogenesis of systemic sepsis. In inflammatory conditions, commensal bacteria exploit transcytotic pathways to cross the intestinal epithelium in a TLR4-dependent manner. The aim of this study was to test the hypothesis that Lactobacillus plantarum ameliorates tumour necrosis factor-induced bacterial translocation by regulation of Toll-like receptor-4 expression.Methodology. L. plantarum strains were investigated to determine their capacity to inhibit the initial adhesion of Escherichia coli B5 to Caco-2 cells. The inhibitory effects of L. plantarum on TNF-alpha-induced E. coli B5 translocation across Caco-2 cells were studied. Barrier function and integrity were simultaneously assessed by transepithelial electrical resistance, HRP permeability, LDH release and distribution of tight junctional proteins. Expression of TLR4 was assessed by RT-PCR.Results/Key findings. Pretreatment of monolayers with L. plantarum L2 led to a significant decrease in E. coli B5 adhesion and cell internalization (P