Oral administration of Lactobacillus plantarum 06CC2 prevents experimental colitis in mice via an anti­inflammatory response.

Dysbiosis of the enteric microbiota causes gastrointestinal diseases, including colitis. The present study investigated the beneficial effect of Lactobacillus plantarum 06CC2 in experimental colitis in mice. An experimental colitis model in C57BL6 mice was induced using dextran sulfate sodium. Mice were orally administered 06CC2 (06CC2 group) or PBS only (control group) by gavage. The disease activity index (DAI), histological grading, and colon tissue and colonic lamina propria mononuclear cells (LPMCs) were examined macroscopically and histopathologically, and the expression levels of inflammation­associated cytokines (IL­6, IL­12, TNF­α and IL­10) in these samples were determined. Compared with the control group, the 06CC2 group exhibited a significantly lower DAI (1.5±0.8 vs. 0.2±0.3, respectively; P<0.05) and pathology score (6.3±1.5 vs. 3.8±1.3, respectively; P<0.05). IL­10 expression in colonic LPMCs was higher in the 06CC2 group than in the control group, although there was no significant difference in IFN­Î³, IL­6 or IL­12 expression in colonic LPMCs between the two groups. In addition, 06CC2 stimulated the production of IL­10 from CD11b­positive cells and CD11c­positive cells in the colon. The 06CC2 strain induced IL­10 production in the colon and attenuated colon inflammation.

A high­fructose diet induces epithelial barrier dysfunction and exacerbates the severity of dextran sulfate sodium­induced colitis.

Excessive fructose intake is a risk factor for gut symptoms in patients with inflammatory bowel disease, however, its effect on the intestinal tract has not been evaluated previously. The present study investigated the impact of a high­fructose diet (HFD) on intestinal barrier function in mice with experimental colitis. C57/BL6 mice were provided with either a HFD or control diet and either plain drinking water or water containing 1% dextran sulfate sodium (DSS) for 2 weeks. The disease activity index (DAI), pathological scores and expression of inflammatory cytokines were compared among the groups, and the proportions of fecal bacteria in the colon were analyzed. The body weight and colon length were significantly decreased, and the DAI and pathological scores were significantly increased in the DSS/HFD­treated mice compared with the non­DSS­treated and control diet mice. Regarding the expression of inflammatory cytokines, the levels of interleukin (IL)­6, IL­1ß and tumor necrosis factor­α were significantly increased, and the expression of the tight junction protein occludin was significantly decreased in the DSS/HFD­treated mice. The total bacterial count was increased in the HFD mice. Taken together, these results indicate that an HFD resulted in the deterioration of intestinal barrier function and increased susceptibility to DSS­induced colitis.

The utility of apoptosis inhibitor of macrophages as a possible diagnostic marker in patients with Crohn's disease.

BACKGROUND: Apoptosis inhibitor of macrophages (AIM) was initially identified as an apoptosis inhibitor that supports the survival of macrophages against various apoptosis-inducing stimuli, and AIM produced by macrophages may contribute to the pathogenesis of inflammatory bowel diseases (IBDs). However, there have been no reports on the kinetics of AIM in IBD and the impact of AIM on the pathogenesis of IBD. In this study, we aimed to investigate the diagnostic utility of levels of AIM and their correlation with the activity of Crohn's disease (CD) and IBD. METHODS: We used an enzyme-linked immunosorbent assay (ELISA) to examine AIM serum levels in 16 healthy subjects and 90 patients with inflammatory bowel diseases, namely 39 with CD and 51 with ulcerative colitis (UC), as well as 17 patients with Behcet's disease (BD) as intestinal disease controls. We compared serum AIM levels among groups and examined whether there were correlations between serum AIM levels and disease activity and type. We also performed immunohistochemical staining of AIM in intestinal tissues of patients with CD. RESULTS: Serum AIM levels were significantly higher in patients with CD than in patients with UC, BD, and controls (3.27 ± 2.14, 1.88 ± 1.43, 2.34 ± 1.37, and 2.13 ± 0.64 µg/ml, respectively; P < 0.01). There was no difference in serum AIM levels before and after treatment in patients with CD. However, in these patients the diagnostic rate using AIM was better than that based on anti-Saccharomyces cerevisiae antibodies. AIM was expressed in macrophages that were positive for CD14, CD16, or both in the intestinal tissues of patients with CD. CONCLUSIONS: AIM is a novel biomarker of CD that can distinguish CD from UC or BD. It is suggested that AIM may contribute to intestinal inflammation by inhibiting the apoptosis of macrophages.