Lacidophilin Modulated Gut Microbiota and Ameliorated Dextran Sulfate Sodium-Induced Mouse Colitis

Abstract The prevalence of inflammatory bowel disease (IBD) has been rising significantly in recent years. It is widely accepted that gut microbes play an essential role in the development of IBD. Lacidophilin is a product of milk fermentation by lactobacillus acidophilus. The aim of this study was to investigate the effect of Lacidophilin on colitis induced by dextran sulfate sodium (DSS). 16s RNA sequencing was performed to determine the changes of species composition and community structure of the intestinal microflora, and transcriptome sequencing was conducted to find out the gene or protein which may be affected by Lactobacillus on colitis development potentially. It was observed that the 7 days administration of Lacidophilin protected the intestinal mucosal barrier from damage, and thereby enabled the remission of colitis severity. Compared to the model group, Lacidophilin could restore the shortened colon length and marked decrease levels of TNF-α and IL-6 in serum. More importantly, Lacidophilin significantly increased the abundance of beneficial bacteria such as Lactobacillus, Bifidobacterium and Lachnospiraceae_NK4A136_group, decreased the abundance of harmful bacteria such as Escherichia-Shigella and Parvibacter. Transcriptomic analysis shows that IL-17 signaling pathway, BCR signaling pathway, Toll-like receptor signaling pathway, and TNF signaling pathway was enriched, and we found that Lcn2, Ccl3, Mmp8, Slc11a1, Spp1, and Serpine1 might be potential targets of Lacidophilin treatment. These studies indicate that Lacidophilin can ameliorate colitis in mice through maintaining the integrity of intestinal structure and improving intestinal microbiota, and its mechanism may be involved in immune-related proteins and pathways.