植物乳杆菌 MYL26 诱导 Caco-2 细胞产生内毒素耐受表型。
Lactobacillus plantarum MYL26 induces endotoxin tolerance phenotype in Caco-2 cells.
机构信息
Department of Food Science and Biotechnology, National Chung Hsing University, Taichung 40227, Taiwan.
出版信息
BMC Microbiol. 2013 Aug 10;13:190. doi: 10.1186/1471-2180-13-190.
BACKGROUND
Crohn's disease and ulcerative colitis are the major types of chronic inflammatory bowel disease occurring in the colon and small intestine. A growing body of research has proposed that probiotics are able to attenuate the inflammatory symptoms of these diseases in vitro and in vivo. However, the mechanism of probiotic actions remains unclear.
RESULTS
Our results suggested Lactobacillus plantarum MYL26 inhibited inflammation in Caco-2 cells through regulation of gene expressions of TOLLIP, SOCS1, SOCS3, and IκBα, rather than SHIP-1 and IRAK-3.
CONCLUSIONS
We proposed that live/ heat-killed Lactobacillus plantarum MYL26 and bacterial cell wall extract treatments impaired TLR4-NFκb signal transduction through Tollip, SOCS-1 and SOCS-3 activation, thus inducing LPS tolerance. Our findings suggest that either heat-killed probiotics or probiotic cell wall extracts are able to attenuate inflammation through pathways similar to that of live bacteria.
背景
克罗恩病和溃疡性结肠炎是发生在结肠和小肠的主要类型的慢性炎症性肠病。越来越多的研究表明，益生菌能够在体外和体内减轻这些疾病的炎症症状。然而，益生菌作用的机制尚不清楚。
结果
我们的结果表明，植物乳杆菌 MYL26 通过调节 TOLLIP、SOCS1、SOCS3 和 IκBα 的基因表达，而不是通过 SHIP-1 和 IRAK-3，抑制 Caco-2 细胞的炎症。
结论
我们提出，活菌/热处理的植物乳杆菌 MYL26 和细菌细胞壁提取物通过 Tollip、SOCS-1 和 SOCS-3 的激活来损害 TLR4-NFκb 信号转导，从而诱导 LPS 耐受。我们的研究结果表明，无论是热处理的益生菌还是益生菌细胞壁提取物，都能够通过类似于活菌的途径来减轻炎症。
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