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

Abstract

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 microbiota depletion and FMT results confirmed the gut microbiota-dependent mechanism as that V_A relieved UC via regulating gut microbiota: increase in SCFA-producing 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.

Keywords: Fecal microbiota transplantation; Gut microbiota; Short-chain fatty acids; Ulcerative colitis; Vitamin A.