Vitamin A supplementation ameliorates ulcerative colitis in gut microbiota-dependent manner

Ulcerative colitis (UC), is a chronic relapsing inflammatory condition of the gastrointestinal track. The purpose of this study is to explore whether Vitamin A (V-A) can treat UC and its mechanisms. A mouse model of UC was established using 3.0% (w/v) dextran sodium sulfate (DSS). V-A was used to treat UC by intragastric administration of 5000 international unit (IU) retinyl acetate. Fecal microbiota transplantation (FMT) was also used to treat the UC model mice to verify the effect of influenced gut microbiota. The content of short-chain fatty acids (SCFAs) in cecal contents was quantitatively detected by gas chromatography and mass spectrometry. V-A supplementation significantly ameliorated UC. 16S rRNA sequencing indicated that V-A-treated mice exhibited much more abundant gut microbial diversity and flora composition. Targeted metabolomics analysis manifested the increased production of SCFAs in V-A-treated mice. Gut micmbiota depletion and FMT results confirmed the gut microbiota-dependent mechanism as that V-A relieved UC via regulating gut microbiota: increase in SCFAproducing genera and decrease in UC-related genera. The restore of intestinal barrier and the inhibition of inflammation were also found to contribute to the amelioration of UC by V-A. It was concluded that a V-A supplement was enough to cause a significant change in gut microbiota and amelioration of UC.

Automated summary

Vitamin A supplementation significantly ameliorated ulcerative colitis by regulating gut microbiota, increasing short-chain fatty acid production, and restoring intestinal barrier and inhibiting inflammation.