Abstract
Inflammatory bowel disease, a gut disease that is prevalent worldwide, is characterized by chronic intestinal inflammation, such as colitis, and disorder of the gut microbiome. Glycine (Gly) is the simplest amino acid and functions as an anti-inflammatory immune-nutrient and intestinal microbiota regulator. This study aimed at investigating the effect of Gly on colitis induced in mice by intrarectal administration of 5% acetic acid (AA). Bodyweight and survival rates were monitored, and colonic length and weight, serum amino acid concentrations, intestinal inflammation-related gene expression, and colonic microbiota abundances were analyzed. The results showed that Gly dietary supplementation had no effect on the survival rate or the ratio of colonic length to weight. However, Gly supplementation reversed the AA-induced increase in serum concentrations of amino acids such as glutamate, leucine, isoleucine, and valine. Furthermore, Gly inhibited colonic gene expression of interleukin- (IL-) 1β and promoted IL-10 expression in colitis mice. Gly supplementation also reversed the AA-induced reduction in the abundance of bacteria such as Clostridia, Ruminococcaceae, and Clostridiales. This change in the intestinal microbiota was possibly attributable to the changes in colonic IL-10 expression and serum concentrations of valine and leucine. In sum, Gly supplementation regulated the serum concentrations of amino acids, the levels of colonic immune-associated gene expression, and the intestinal microbiota in a mouse model of colitis. These findings enhance our understanding of the role of Gly in regulating metabolism, intestinal immunity, and the gut microbiota in animals afflicted with colitis.
Highlights
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is characterized by a loss of intestinal mucosal homeostasis associated with inappropriate and aggravated immune responses to intestinal lumen antigens [1,2,3]
Previous studies demonstrated that acetic acid (AA)-induced colitis might be a good model with which to study the efficacy of drugs [9], so we used AA to induce colitis in this study
We evaluated the effect of GLY on AA-induced colitis in mice by comparing the survival rate and the ratio of colonic weight to length
Summary
Inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), is characterized by a loss of intestinal mucosal homeostasis associated with inappropriate and aggravated immune responses to intestinal lumen antigens [1,2,3]. It is widely believed that IBD is caused by complex interactions between genetic and environmental factors, such as immune-response disorders and microbial community changes. The cause of IBD remains unclear, and further research is needed [5, 6]. Several types of pharmacologically induced animal colitis models have been developed, such as dextran sulfate- (DSS-), trinitrobenzene sulfonic acid- (TNBS-), or acetic acid- (AA-) induced models [7, 8]. DSS is widely used for this purpose, as is TNBS, typically in combination with ethanol. Previous studies demonstrated that AA-induced colitis might be a good model with which to study the efficacy of drugs [9], so we used AA to induce colitis in this study
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