Abstract
Simple SummaryInflammatory bowel disease (IBD) is extremely harmful to animal health and can affect animal growth and production. Dextran sulfate sodium (DSS) can cause IBD in animals, resulting in diarrhea and bloody stools. The present study aimed to determine whether oral sodium butyrate can relieve DSS-induced colitis in mice. By using histological evaluation (H&E) staining technology and 16S rRNA sequence analysis, we found that the severity of colitis in mice receiving oral sodium butyrate was reduced, and the composition of gut microbiota was changed. These results indicate that sodium butyrate can relieve DSS-induced colitis in mice by restoring the balance of gut microbiota dysbiosis.Inflammatory bowel disease (IBD) develops as a result of complicated interactions between genetic susceptibility, excessive innate immunity, and environmental factors, which are mainly related to the gut microbiota. The present study aimed to elucidate the protective effects and underlying mechanisms of a short-chain fatty acid salt, sodium butyrate, on colonic inflammation induced by dextran sulfate sodium (DSS) in mice. Pretreatment with sodium butyrate attenuated colitis, as demonstrated by the decreased disease activity index (DAI), colon length shortening, spleen tumidness, and histopathology scores, while maintaining intestinal barrier integrity, as observed by H&E staining and electron microscopy. 16S rRNA sequence analysis revealed that sodium butyrate caused a remarkable alteration of the gut microbiota. Bacteroides, Lachnospiraceae, the Lachnospiraceae NK4A136 group, and Ruminiclostridium 6 presented dramatic differences after sodium butyrate supplementation. This work verifies that sodium butyrate can improve mouse colitis via microbe–host interactions by regulating the microbial community. Taken together, the findings demonstrate that sodium butyrate shows great potential as a probiotic agent for ameliorating colitis.
Highlights
Inflammatory bowel disease (IBD) is an autoimmune disease characterized by a chronic inflammatory status resulting from an abnormal immune response
To define whether NaB played a protective role against colitis in vivo, a series of clinical signs of colitis were monitored in the dextran sulfate sodium (DSS)-induced mice, including their weight, stool consistency, and rectal bleeding
Relative to the Con and DSS groups, there was a higher abundance of Cyanobacteria, Deferribacteres, and Tenericutes in the NaB-treated mice. These results demonstrated that oral NaB had beneficial effects on the dysbiosis of the gut microbiota caused by DSS treatment at the phylum level
Summary
Inflammatory bowel disease (IBD) is an autoimmune disease characterized by a chronic inflammatory status resulting from an abnormal immune response. The immune system and microbiota of the intestine maintain intestinal homeostasis to improve intestinal development [3]. The incidence of IBD has previously been related to dietary patterns and additives that modulate the gut microbiota [6,7,8]. Short-chain fatty acids (SCFAs), which are mainly produced by the cecal fermentation of nonstarch polysaccharides, play crucial roles in maintaining colon pH and osmolarity [9].
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