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Metabolic profiling of the fecal extracts of male mice was carried out to assess the effects of probiotics on colonic inflammation using 1H NMR spectroscopy coupled with multivariate data analysis. The control group (n = 5) was administered phosphate buffered saline for 14 days. Acute colitis was induced with dextran sulfate sodium (DSS) for 7 days following administration of phosphate buffered saline for 7 days (DSS-treated group, n = 5). LAB + DSS-treated group (n = 5) was administered lactic acid bacteria (LAB) daily for 7 days followed by treatment with DSS for 7 days to investigate protective effect of LAB against DSS-inducible colitis. Histological damage, myeloperoxidase activity, and malondialdehyde content of colon tissue were reduced, whereas colon length increased in LAB + DSS-treated mice compared to those in DSS-treated mice. DSS treatment was associated with fecal excretion of amino acids, short chain fatty acids, and nucleotides, revealing significant decreases of threonine, alanine, glutamate, glutamine, aspartate, lysine, glycine, butyrate, uracil, and hypoxanthine together with increases of monosaccharides, glucose, and trimethylamine in the feces of mice with DSS-induced colitis. Increased levels of acetate, butyrate, and glutamine and decreased levels of trimethylamine were found in the feces of LAB + DSS-treated mice compared to DSS-treated mice alone. The increased short chain fatty acids levels in the feces of mice fed with LAB indicate that the probiotics have protective effects against DSS-induced colitis via modulation of the gut microbiota. This work highlights the possibility for alternative approach of metabonomics in feces for assessing the probiotic effect in an animal model of inflammatory bowel disease. [ABSTRACT FROM AUTHOR]

To investigate the mechanisms of the preventive activity of lactic acid bacteria in colitis, the inhibitory effect of Bifidobacterium longum HY8004, which potently inhibited lipid peroxidation in vitro, was examined in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice. We measured the ability of lactic acid bacteria (LAB) to inhibit lipid peroxidation in vitro and to inhibit colitis outcomes, colon shortening, and myeloperoxidase activity in TNBS-induced colitis in C3H/HeN and C3H/HeJ mice. We also measured levels of the inflammatory markers interleukin (IL)-1β and tumor necrosis factor (TNF)-α and their transcription factor, NF-κB, in the colon by enzyme-linked immunosorbent assay and immunoblot analysis. Among the LAB tested, B. logum HY8004 most potently inhibited lipid peroxidation in vitro but did not inhibit TLR-4-linked NF-κB activation in HEK cells. Oral administration of HY8004 inhibited TNBS-induced colon shortening and myeloperoxidase activity in the colon of C3H/HeN and C3H/HeJ mice as well as IL-1β and TNF-α expression. B. longum HY8004 also inhibited TNBS-induced lipid peroxidation, TLR-4 expression, and NF-κB activation in the colon of C3H/HeN and C3H/HeJ mice. B. longum HY8004 can improve colitis via the inhibition of lipid peroxidation as well as NF-κB activation. [ABSTRACT FROM AUTHOR]

The purpose of this study is to investigate the immuno-stimulatory function of the lactic acid bacteria (LAB), Lactobacillus plantarum HY7712, isolated from kimchi. When NF-κB-activating activities of 200 LAB isolated from kimchi were measured in RAW264.7 cells stimulated with or without LPS, L. plantarum HY7712 most potently induced NF-κB activation in RAW264.7 cells, while the presence of LPS induced inhibition of NF-κB activation. HY7712 also induced the expression of IL-12 and TNF-α, transcription factor for NF-κB, in human PBMCs. In order to investigate the effect of toll-like receptor (TLR)-associated HY7712-signaling pathway, psiTLR2- or psiTLR4-transfected RAW264.7 cells were used to measure the NF-κB activation with the same stimulation with HY7712. HY7712 activated NF-κB in wild-type and psiTLR4-knockout cells, but not in psiTLR2-knockout cells, indicating HY7712 can activate Raw264.7 cell via TLR2/NF-κB signaling. In addition, HY7712 induced the expression of IL-12 and IFN-γ in mouse splenocytes, and also the activation markers CD80, 86, and MHC class II in mouse bone marrow-derived dendritic cells. [ABSTRACT FROM AUTHOR]