title: Multistep mechanism of probiotic bacterium, the effect on innate immune system.
abstract: The etiology and pathogenesis of inflammatory bowel disease are still not fully understood. However, evidence from both animal models and clinical observations suggests luminal bacteria as the most probable inducer of this disease. The intestinal bacterial microbiota may be modified by dietary addition of viable probiotic bacteria, thereby constituting an alternative approach to disease prevention and treatment. The aim of this study was to evaluate and compare the effects of two probiotic regiments; Lactobacillus GG and a mixture of Streptococcus thermophilus, Lactobacillus acidophilus, and Bifidobacterium lactis (YO-MIX Y 109 FRO 1000) in both normal and trinitrobenzenesulfonic acid colitis-induced rats. Colon morphology and damage were evaluated histologically; colonic tissues were used for mRNA analysis, using real-time PCR. Administration of both probiotics reduced the expression of proinflammatory cytokines tumor necrosis factor-alpha and IL-6 and increased the expression of mucin 2 in compared with colitis group and reduced the inflammatory response. These results provide additional support for the positive effect of probiotics in the gut and may shed light on the mechanism by which probiotic bacteria exert their action in an animal model.
authors.affiliation: Department of Animal Science, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, Rehovot 76100, Israel.
authors.forename: Einat
authors.initials: E
authors.lastname: Amit-Romach
authors.forename: Zehava
authors.initials: Z
authors.lastname: Uni
authors.forename: Ram
authors.initials: R
authors.lastname: Reifen
mesh_terms: D000818:Animals; D001644:Bifidobacterium; D003092:Colitis / Q000139:chemically induced / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D003106:Colon / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D005786:Gene Expression Regulation; D007113:Immunity, Innate; D018836:Inflammation Mediators / Q000378:metabolism; D015212:Inflammatory Bowel Diseases / Q000276:immunology / Q000628:therapy; D007778:Lactobacillus; D008297:Male; D055262:Mucin-2 / Q000235:genetics / Q000378:metabolism; D020556:Neutrophil Infiltration; D019936:Probiotics / Q000494:pharmacology* / Q000627:therapeutic use; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013291:Streptococcus; D051195:Toll-Like Receptor 2 / Q000235:genetics / Q000378:metabolism; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D023083:beta-Defensins / Q000235:genetics / Q000378:metabolism
chemical_list: D018836:Inflammation Mediators; C524628:Muc2 protein, rat; D055262:Mucin-2; D012333:RNA, Messenger; C495343:Tlr2 protein, rat; C495347:Tlr4 protein, rat; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D023083:beta-Defensins; C549474:beta-defensin-2, rat