Ethanolamine improves colonic barrier functions and inflammatory immunoreactions via shifting microbiome dysbiosis

Ethanolamine(EA) often occurs at a relatively high concentration within the inflamed gut of IBD patients. To investigate the role of EA in colonic inflammation and host-microbiome dysbiosis, thirty-six ICR mice were treated with 3% DSS for a week to generate acute intestinal inflammation and then supplied with 0 μM, 500 μM (LowEA), and 3000 μM (HighEA) in drinking water for two weeks, after that, 16s RNA sequencing was applied in characterizing the changes in colonic microbiota driven by different EA levels. An inflamed colonic organoid model via 3% DSS treatment was also established for further verification of these in vivo findings. EA significantly reduced proximal colonic crypt depth but increased distal colonic villus height in HighEA group. The protein and mRNA expression of occludin and Reg3β, BD1, BD2, and MUC2 were significantly up-regulated in EA treated groups. EA decreased mucosal inflammation-related cytokines levels (IL1, IL6, IL17, TNFα, and INFγ) and increased the significantly increased concentration of sIgA. Serum aspartate aminotransferase and alanine aminotransferase were significantly down-regulated in the highEA group. EA increased the relative abundance of Blautia, Roseburia, Lactobacillus, Faecalibaculum, Candidatus_Saccharimonas, Alloprevotella, and Lachnoclostridum and thus microbial metabolic pathways including Oxidative phosphorylation, Lipopolysaccharide biosynthesis, Arginine and proline metabolism, Folate biosynthesis, and Biotin metabolism were more abundant in LowEA group than those in control. EA up-regulated the protein or mRNA expression of TLR4/MyD88 in colonic tissues and the DSS-treated colonic organoid model. This study firstly demonstrated that ethanolamine in altering host-microbiome dysbiosis, which may provide new insights into the role of dietary lipids in IBD.