Lactobacillus plantarum MYL26 induces endotoxin tolerance phenotype in Caco-2 cells.
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.
Department of Food Science and Biotechnology, National Chung Hsing University, Taichung 40227, Taiwan.
Yi-Heng
YH
Chiu
Ying-Chen
YC
Lu
Chu-Chyn
CC
Ou
Shiao-Lin
SL
Lin
Chin-Chi
CC
Tsai
Chien-Tsai
CT
Huang
Meei-Yn
MY
Lin
D018938:Caco-2 Cells; D004731:Endotoxins / Q000276:immunology*; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D007422:Intestines / Q000187:drug effects / Q000276:immunology* / Q000382:microbiology; D048191:Lactiplantibacillus plantarum / Q000737:chemistry / Q000502:physiology*; D008070:Lipopolysaccharides / Q000276:immunology; D010641:Phenotype; D019936:Probiotics / Q000494:pharmacology*
D004731:Endotoxins; D008070:Lipopolysaccharides