Clostridium butyricum alleviates dextran sulfate sodium-induced experimental colitis and promotes intestinal lymphatic vessel regeneration in mice

Abstract

Background: Inflammatory bowel disease (IBD) is the most common precancerous lesion of colitisassociated colon cancer (CAC). Studies have confirmed that pathological changes in intestinal lymphatic vessels (LVs) significantly promoted the development of IBD-associated carcinogenesis. An imbalance in the microecology of the intestinal flora is a key factor in the progression of IBD. As a result, therapeutic techniques that focus on the relationship between LV regeneration and flora management might be a potential treatment strategy. Methods:We investigated the role of Clostridium butyricum (C butyricum) in a dextran sulfate sodium (DSS)-induced IBD mouse model. Balb/c mice were given 3% DSS in their drinking water for 8 days to produce acute colitis and simultaneously administrated with C butyricum for 12 days. Hematoxylin and eosin (H&E) staining was used to evaluate the degree of colitis tissue damage. Levels of the lymphatic endothelial cell (LEC)-specific marker LYVE-1 and intestinal expressions of pro-lymphatic vascular endothelial growth factor (VEGF)-C and VEGF-D were determined using immunohistochemical assays.Results: In a DSS-induced IBD mouse model, we found that butyric acid-producing C butyricum significantly reduced disease activity index (DAI) scores in mice, reversed the shortening of the colon, weakened the degree of damage to colonic epithelial tissues, inhibited lymphocyte infiltration, and reduced pathological damage to the colon. To our knowledge, this is the first time that tissue expressions of LYVE-1, VEGF-C, and VEGF-D have been seen to increase in IBD-model mice after treatment with C butyricum.Conclusions: Our findings suggest that C butyricum might alleviate IBD in DSS-induced IBD-model mice by promoting intestinal LV regeneration.

Pretreatment with an antibiotics cocktail enhances the protective effect of probiotics by regulating SCFA metabolism and Th1/Th2/Th17 cell immune responses

“…For instance, some probiotics have proved to be therapeutic against non-alcoholic fatty liver disease (NAFLD) and dysbiosis-induced diarrhea [ 7 , 34 ]. Herein, CBM can relieve the intestinal inflammation on weight loss, gut barrier injury, and histological injury of colitis mice effectively, which is consistent with previous studies [ 35 , 36 ].…”

Clostridium butyricum and Chitooligosaccharides in Synbiotic Combination Ameliorate Symptoms in a DSS-Induced Ulcerative Colitis Mouse Model by Modulating Gut Microbiota and Enhancing Intestinal Barrier Function

“…The method of Chen et al ( 10 ), with minor modification, was used to conduct immunohistochemical analysis. Colon tissue sections were deparaffinized, rehydrated, treated with citrate buffer (pH 6.0) for antigen retrieval, washed with phosphate-buffered saline (PBS), incubated in 3% H 2 O 2 to eliminate endogenous peroxidase activity, blocked with goat serum, incubated with anti-ZO-1 (catalog no.…”

Exploring Gut Microenvironment in Colorectal Patient with Dual-Omics Platform: A Comparison with Adenomatous Polyp or Occult Blood

“…In contrast, supplementation of dietary fiber led to increases in the gut short-chain fatty acids (SCFAs), including acetic acid, propionic acid, and butyric acid, which are metabolized by Faecalibaculum rodentium and Clostridium butyricum [ 41 , 42 ]. Published reports documented that combined supplementation of diverse SCFAs or SCFA-generated flora diminished tumor formation or lessened colonic inflammation in a mouse model [ 43 , 44 ]. In addition to the identification of CRC-enriched metabolites in fecal samples, the metabolite-species association was assessed by using the ZINB regression model.…”