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.
CITATION STYLE
Zhu, W., Yan, J., Zhi, C., Zhou, Q., & Yuan, X. (2019). 1,25(OH) 2 D 3 deficiency-induced gut microbial dysbiosis degrades the colonic mucus barrier in Cyp27b1 knockout mouse model. Gut Pathogens, 11(1). https://doi.org/10.1186/s13099-019-0291-z
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