Bifidobacterium adolescentis IM38 ameliorates high-fat diet–induced colitis in mice by inhibiting NF-κB activation and lipopolysaccharide production by gut microbiota

• Published in: Nutrition research (New York, N.Y.) Vol. 41; pp. 86 - 96
• Main Authors: Lim, Su-Min, Kim, Dong-Hyun
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2017
• Subjects: Animals; Bifidobacterium adolescentis; Caco-2 Cells; Colitis; Colitis - microbiology; Colitis - therapy; Colon - metabolism; Colon - microbiology; Cytokines - metabolism; Diet, High-Fat - adverse effects; Disease Models, Animal; Gastroenterology and Hepatology; Gastrointestinal Microbiome; Gut microbiota; Humans; Lipopolysaccharide; Lipopolysaccharides - metabolism; Macrophages, Peritoneal - metabolism; Male; Mice; Mice, Inbred C57BL; NF-kappa B - antagonists & inhibitors; NF-kappa B - metabolism; NF-κB activation; Obesity; Obesity - microbiology; Obesity - therapy; Probiotics; Tight Junction Proteins - metabolism; Weight Gain; Gut microbiota; NF- κB activation; COX-2; JNK; cyclooxygenase-2; HFD; LFD; TNF; LPS; mitogen-activated protein kinase; SD; CFU; TAK1; ANOVA; Bifidobacterium adolescentis; Lipopolysaccharide; limulus amoebocyte lysate; iNOS; NF- κB; interleukin; inducible nitric oxide synthetase; Th17; c-jun N-terminal kinase; one-way analysis of variance; Obesity; general anaerobic medium; transforming growth factor β–activated kinase 1; IL; regulatory T; Treg; low-fat diet; MAPK; GAM; extracellular signal–related kinase; tumor necrosis factor; LAL; helper T17; enzyme-linked immunosorbent assay; high-fat diet; colony-forming unit; Colitis; nuclear factor–kappa B; ELISA; ERK; standard deviation; NF-κB; NF-κB activation
• ISSN: 0271-5317; 1879-0739
• DOI: 10.1016/j.nutres.2017.04.003

Abstract Gut microbiota play essential roles in the regulation of human metabolism via symbiotic interactions with the host. Prolonged consumption of high-fat diet (HFD) elevates the Firmicutes to Bacteroidetes ratio and lipopolysaccharide (LPS) production by gut microbiota, thereby increasing the probability of developing metabolic and immune disorders such as obesity and colitis. The use of probiotics with anti-inflammatory properties has been suggested to counteract this effect. Here, we tested whether Bifidobacterium adolescentis IM38, which inhibited nuclear factor–kappa B (NF- κ B) activation in Caco-2 cells and peritoneal macrophages and inhibited Escherichia coli LPS production, exerted an anticolitic effect in mice with HFD-induced obesity. Oral administration of IM38 (2 × 109 CFU/mouse per day) for 6 weeks in mice with HFD-induced obesity inhibited whole-body and epididymal fat weight gain. IM38 also increased HFD-suppressed expression of interleukin (IL)-10 and tight junction proteins but significantly downregulated HFD-induced NF- κ B activation and tumor necrosis factor expression in the colon. IM38 inhibited differentiation into helper T17 cells and reduced IL-17 levels in the colon of mice with HFD-induced obesity but increased HFD-suppressed differentiation into regulatory T cells and IL-10 levels. Furthermore, treatment with IM38 lowered the HFD-induced LPS levels in blood and colonic fluid, as well as the Proteobacteria to Bacteroidetes ratio in gut microbiota. Therefore, we suggest that IM38 can inhibit HFD-induced LPS production in gut microbiota through the regulation of Proteobacteria to Bacteroidetes ratio and NF- κ B activation in the colon, which ultimately attenuates colitis. Thus, IM38 may be a suitable ingredient of functional foods designed for treating or preventing colitis.