Role of lactobacillus and bifidobacterium in the enhancement of epithelial barrier function and anti-inflammation induced by gastrointestinal bacterial pathogens

Abstract

Specific strains of Lactobacillus spp. and Bifidobacterium spp. can enhance epithelial barrier function and prevent pathogen-induced damage of epithelial tight junctions (TJs) and anti-inflammation induced by gastrointestinal bacterial pathogens. We screened indigenous Lactobacillus and Bifidobacterium Thai isolates with the ability to increase the integrity ofTJs by transepithelial electrical resistance (TER) assay in Caco-2 cells. Eight Lactobacillus isolates (LF-LI2, LO-NL49, LM-B57, LP-XB7, LS-B37, LSB60, LR-L34 and LC-L39) and three Bifidobacterium isolates (BA-B24, BB-NB42 and BP-NB48) can prevent the destruction of TJs by Clostridium difficile. LR-L34 which was selected for further investigation had the ability to improve the intestinal epithelial barrier destroyed by C. difficile although the magnitude of improvement is lower than that of protection. LR-L34 also had protective effect on the destruction of TJs by Campylobacter jejuni but not by Vibrio cholerae 0 I I naba and Salmonella Typhimurium . LR-L34 was able to increase the expression of claudin-l significantly and its pretreatment prevented C. difficile-induced decrease in the expression of claudin-I and occludin significantly. Furthermore, LR-L34 has the ability to suppress C. difficileinduced interleukin-8 (IL-8) production. Further investigation of BB-NB42 demonstrated that it prevented the damage of TJ integrity by C. jejuni and S. Typhimurium but not by V.cholerae 01 Inaba. BB-NB42 increased the expression of claudin-I and occludin significantly and its pretreatment prevented the decrease in expression of claud in-I , JAMI and occludin significantly. However, BB-NB42 does not have the ability to suppress C. difficile-induced IL-8 production.