Lactobacillus plantarum MYL26 induces endotoxin tolerance phenotype in Caco-2 cells
1 Department of Food Science and Biotechnology, National Chung Hsing University, 250 Kuokuang Road, Taichung 40227, Taiwan
2 Department of Food Science, National Chiayi University, Chiayi City, Taiwan
3 School of Nutrition, Chung Shan Medical University, Taichung, Taiwan
4 Department of Nutrition, Chung Shan Medical University Hospital, Taichung, Taiwan
5 Department of Neurology, Chong Guang Hospital, MiaoLi County, Taiwan
BMC Microbiology 2013, 13:190 doi:10.1186/1471-2180-13-190Published: 10 August 2013
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.
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.
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.