Evidence suggests that gut microbiota dysbiosis plays a critical role in the initiation and promotion of inflammatory bowel disease (IBD). Kefir is a fermented dairy product including yeast and bacterial species. We aimed to investigate the effect of kefir on trinitrobenzene sulfonic acid (TNBS)‐induced colitis in rats using two different doses. Fifty‐four Wistar rats were divided into six groups. For 14 days, the normal control and colitis control groups were given tap water, kefir10 control, kefir10 colitis, and kefir30 control, and the kefir30 colitis groups were given phosphate‐buffered saline containing 10% or 30% kefir, respectively, instead of tap water. Colitis was induced by intracolonically administrating TNBS in the colitis control, kefir10 colitis, and kefir30 colitis groups. On the 14th day, the rats were sacrificed. The weights and lengths of the colons were measured and macroscopically evaluated, and the distal 10 cm segments were subjected to a histopathological examination. The incidence of bloody stool and diarrhea in the kefir10 colitis group was found to be less than the colitis control and kefir30 colitis groups. The colonic weight/length ratio in the kefir10 colitis group was lower than that in the colitis control and kefir30 colitis groups. We detected that the 10% kefir treatment reduced TNBS‐induced macroscopic colonic damage, while it was exacerbated by the 30% kefir treatment. No significant difference was observed between the colitis groups in terms of microscopic colonic damage scoring. These results indicate that kefir, with a careful dose selection, may be a useful agent in the treatment of IBD.
The protective effect of a probiotic mixture of 13 different bacteria and α-tocopherol on 98% ethanol-induced gastric mucosal injury was evaluated. Levels of gastric mucosal pro- and anti-inflammatory cytokines, malondialdehyde, and secretory immunglobulin A were measured. Rats were allocated into four groups: control, ethanol, probiotic, and α-tocopherol. The control and ethanol groups received skim milk for 14 days. Probiotic and α-tocopherol groups were administered probiotic mixture suspended in skim milk and 100 mg/kg α-tocopherol, respectively, by daily gavage for 14 days. On Day 15, gastric lesions were induced by administration of ethanol 98% (1 mL) to all rats except those in the control group. Probiotic, but not α-tocopherol, seemed to inhibit ethanol-induced gastric mucosal tumor necrosis factor-α, interferon-γ, and interleukin-2 production (P > .05). Ethanol caused the elevation of mucosal interleukin-4 level (compared to the control, P < .05). Probiotic pretreatment significantly suppressed the ethanol-induced increase of gastric mucosal interleukin-4 levels. Pretreatment with either probiotic or α-tocopherol inhibited the ethanol-induced increase of mucosal malondialdehyde concentration (P < .01 and P < .05, respectively). Probiotic pretreatment enhanced the gastric mucosal secretory immunoglobulin A concentration (P < .001). In conclusion, probiotic mixture and α-tocopherol reduced ethanol-induced gastric mucosal lipid peroxidation, suggesting that they may be beneficial for gastric lesions induced by lower ethanol concentration.
Brucellosis may lead to complications that affect different organ systems, including the liver and spleen. In acute disease, hepatosplenic abscess is a rare complication. We report herein a woman with splenic abscess due to acute Brucella melitensis infection who was successfully treated with antibiotics alone.
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