Significance and Impact of the Study: Colistin has been reported to be effective in selective digestive decontamination (SDD), which is an infection prevention measure used in the treatment of certain patients in intensive care. We are the first to report that colistin-induced intestinal dysbacteriosis can injure intestinal mucosal barrier function and increase bacterial translocation, whereas a high dose of colistin does not damage the intestinal mucosal barrier in germ-free (GF) mice raised in a GF environment. These results may indicate that prolonged use of a high dose of a SDD medication should be carefully considered. AbstractThe purpose of this study was to determine the effect of colistin-induced intestinal dysbacteriosis on intestinal mucosal barrier function and bacterial translocation in a mouse model. Colistin or saline was administered orally for 7 days, and populations of viable organisms from the caecal mucosa and its content, the ileal segments, the mesenteric lymph nodes (MLNs) and the internal organs were prepared for examination. In the intestinal dysbacteriosis model, intestinal barrier dysfunction was observed and associated with increased bacterial translocation to extraintestinal sites. The extent of bacterial translocation to the MLNs and internal organs in the colistin group was significantly higher than in the saline group. Colistin-induced intestinal dysbacteriosis was shown to injure the intestinal mucosa barrier function and increase bacterial dislocation.
Background The relationship between disturbances of the gut microbiota and 1,25(OH) 2 D 3 deficiency has been established both in humans and animal models with a vitamin D poor diet or a lack of sun exposure. Our prior study has demonstrated that Cyp27b1 − / − ( Cyp27b1 knockout) mice that could not produce 1,25(OH) 2 D 3 had significant colon inflammation phenotypes. However, whether and how 1,25(OH) 2 D 3 deficiency due to the genetic deletion controls the gut homeostasis and modulates the composition of the gut microbiota remains to be explored. Results 1,25(OH) 2 D 3 deficiency impair the composition of the gut microbiota and metabolite in Cyp27b1 − / − mice, including Akkermansia muciniphila, Solitalea Canadensis , Bacteroides - acidifaciens , Bacteroides plebeius and SCFA production. 1,25(OH) 2 D 3 deficiency cause the thinner colonic mucus layer and increase the translocation of the bacteria to the mesenteric lymph nodes. We also found 1,25(OH) 2 D 3 supplement significantly decreased Akkermansia muciniphila abundance in fecal samples of Cyp27b1 − / − mice. Conclusion Deficiency in 1,25(OH) 2 D 3 impairs the composition of gut microbiota leading to disruption of intestinal epithelial barrier homeostasis and induction of colonic inflammation. This study highlights the association between 1,25(OH) 2 D 3 status, the gut microbiota and the colonic mucus barrier that is regarded as a primary defense against enteric pathogens.
Plant-derived microRNAs (miRNAs) play a significant role in human health and are “dark nutrients”, as opposed to traditional plant nutrients, as well as important components of food diversification. Studies have revealed that multiple plant-derived miRNA pathways affect human health. First, plant miRNAs regulate plant growth and development and accumulation of metabolites, which alters the food quality and thus indirectly interferes with the health of the host. Moreover, when absorbed in vivo, some miRNAs may target the host cell mRNAs to affect protein expression. In addition, plant miRNAs target and reshape the human gut microbiota (GM), which interferes with the physiology and metabolism of the host. Therefore, miRNAs play a significant role in the cross-kingdom communication of plants, GM, and the host and in maintaining a balance of the three. Future contributions of plant miRNAs can bring new perspectives and opportunities to better understand food nutrition and health care research, which will facilitate the right exploitation of plant resources.
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