Vitamin A deficiency suppresses CEACAM1 to impair colonic epithelial barrier function via downregulating microbial-derived short-chain fatty acids

Yan, Junyan; Xiao, Lü; Feng, Di; Chen, Baolin; Yang, Ting; Tong, Bei; Luo, Ruibang; Wang, Yuting; Chen, Jie

doi:10.1016/j.gendis.2023.03.032

Cited by 9 publications

(3 citation statements)

References 47 publications

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“…In addition to activating Hcar2, butyric acid acts as an inhibitor of histone deacetylase (HDAC), which reduces histone acetylation and stimulates gene expression in host cells [ 67 ]. Recent studies have reported that butyric acid improves the expression of tight junction proteins and intestinal barrier function by inhibiting histone acetylation [ 33 , 68 ]. However, more studies are required to confirm whether the combination of AI-2 with LGG modulates the intestinal barrier function by inhibiting HDAC via butyric acid.…”

Section: Discussionmentioning

confidence: 99%

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Autoinducer-2 promotes the colonization of Lactobacillus rhamnosus GG to improve the intestinal barrier function in a neonatal mouse model of antibiotic-induced intestinal dysbiosis

Hu,

Yang,

et al. 2024

J Transl Med

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Background Human health is seriously threatened by antibiotic-induced intestinal disorders. Herein, we aimed to determine the effects of Autoinducer-2 (AI-2) combined with Lactobacillus rhamnosus GG (LGG) on the intestinal barrier function of antibiotic-induced intestinal dysbiosis neonatal mice. Methods An antibiotic-induced intestinal dysbiosis neonatal mouse model was created using antibiotic cocktails, and the model mice were randomized into the control, AI-2, LGG, and LGG + AI-2 groups. Intestinal short-chain fatty acids and AI-2 concentrations were detected by mass spectrometry and chemiluminescence, respectively. The community composition of the gut microbiota was analyzed using 16S rDNA sequencing, and biofilm thickness and bacterial adhesion in the colon were assessed using scanning electron microscopy. Transcriptome RNA sequencing of intestinal tissues was performed, and the mRNA and protein levels of HCAR2 (hydroxycarboxylic acid receptor 2), claudin3, and claudin4 in intestinal tissues were determined using quantitative real-time reverse transcription PCR and western blotting. The levels of inflammatory factors in intestinal tissues were evaluated using enzyme-linked immunosorbent assays (ELISAs). D-ribose, an inhibitor of AI-2, was used to treat Caco-2 cells in vitro. Results Compared with the control, AI-2, and LGG groups, the LGG + AI-2 group showed increased levels of intestinal AI-2 and proportions of Firmicutes and Lacticaseibacillus, but a reduced fraction of Proteobacteria. Specifically, the LGG + AI-2 group had considerably more biofilms and LGG on the colon surface than those of other three groups. Meanwhile, the combination of AI-2 and LGG markedly increased the concentration of butyric acid and promoted Hcar2, claudin3 and claudin4 expression levels compared with supplementation with LGG or AI-2 alone. The ELISAs revealed a significantly higher tumor necrosis factor alpha (TNF-α) level in the control group than in the LGG and LGG + AI-2 groups, whereas the interleukin 10 (IL-10) level was significantly higher in the LGG + AI-2 group than in the other three groups. In vitro, D-ribose treatment dramatically suppressed the increased levels of Hcar2, claudin3, and claudin4 in Caco-2 cells induced by AI-2 + LGG. Conclusions AI-2 promotes the colonization of LGG and biofilm formation to improve intestinal barrier function in an antibiotic-induced intestinal dysbiosis neonatal mouse model.

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Section: Discussionmentioning

confidence: 99%

“…Caco-2 cell culture and adhesion assays were performed as previously described with minor modifications [ 33 – 35 ]. Caco-2 cells were inoculated into 12-well plates at a concentration of 2*10 5 cells/well and cultured in DMEM medium containing 10% fetal bovine serum until monolayers were formed, and 0.9% saline was rinsed twice.…”

Section: Methodsmentioning

confidence: 99%

Autoinducer-2 promotes the colonization of Lactobacillus rhamnosus GG to improve the intestinal barrier function in a neonatal mouse model of antibiotic-induced intestinal dysbiosis

Hu,

Yang,

et al. 2024

J Transl Med

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“…Microorganisms such as Rosella, Paramecium, Post-Rosella, Staphylococcaceae and Bacillariophyta in the mutant group significantly affected distant metastasis of CRC through KRAS gene mutation, and their prevalence and metastasis were significantly higher than those in the non-mutant group ( Liu et al., 2021 ). Furthermore, butyrate, a prominent component among SCFAs, plays a pivotal role in the metabolic processes of normal colorectal epithelial cells ( Yan et al., 2024 ). Remarkably, a substantial portion of butyrate remains unmetabolized, largely attributed to the fact that colon cells have a Warburg effect pathway ( Eslami et al., 2020 ).…”

Section: Metastasis and Immune Escape Of Crc Cellsmentioning

confidence: 99%

Gut microbiome: decision-makers in the microenvironment of colorectal cancer

Han,

Zhang,

Zhang

et al. 2023

Front. Cell. Infect. Microbiol.

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Colorectal cancer (CRC) is a common malignancy of the gastrointestinal tract, accounting for the second most common cause of gastrointestinal tumors. As one of the intestinal barriers, gut bacteria form biofilm, participate in intestinal work, and form the living environment of intestinal cells. Metagenomic next-generation sequencing (mNGS) of the gut bacteria in a large number of CRC patients has been established, enabling specific microbial signatures to be associated with colorectal adenomato-carcinoma. Gut bacteria are involved in both benign precursor lesions (polyps), in situ growth and metastasis of CRC. Therefore, the term tumorigenic bacteria was proposed in 2018, such as Escherichia coli, Fusobacterium nucleatum, enterotoxigenic Bacteroides fragilis, etc. Meanwhile, bacteria toxins (such as cytolethal distending toxin (CDT), Colibactin (Clb), B. fragilis toxin) affect the tumor microenvironment and promote cancer occurrence and tumor immune escape. It is important to note that there are differences in the bacteria of different types of CRC. In this paper, the role of tumorigenic bacteria in the polyp-cancer transformation and the effects of their secreted toxins on the tumor microenvironment will be discussed, thereby further exploring new ideas for the prevention and treatment of CRC.

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Vitamin A deficiency triggers colonic methylation potentially impairing colonic neuron via downregulation SGK1/FOXO pathway

Tong,

Yan,

Sun

et al. 2024

Pediatric Discovery

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DNA methylation is widely involved in the modification of intestinal function, but the methylation mechanism in the enteric nervous system has not been studied in vitamin A deficiency (VAD). Herein, we firstly found that in the VAD group, gastrointestinal transit time was delayed compared with the vitamin A normal (VAN) group. RNA sequencing between VAD and VAN rats identified enriched pathways associated with enteric nerves and methylation transferase complexes. Then expression levels of DNA methyltransferases (DNMT1, DNMT3a and DNMT3b) were validated to significant increase in the VAD group. Representative reduced bisulfate sequencing showed that the VAD rats had high levels of DNA methylation in promoters and exons compared with the VAN rats. A combined methylomic and transcriptomic analysis identified that methylation levels of Sgk1, a key gene associated with enteric neural development, were elevated in the VAD group, and the activity of the SGK1/FOXO signaling axis was reduced. Furthermore, the colonic neuronal morphology and synaptic architecture were impaired in the VAD offspring. Interestingly, the above alterations in the VAD group were alleviated by vitamin A (VA) supplementation in the early postnatal period. These data suggest that VAD triggers colonic hypermethylation, which probably downregulates the SGK1/FOXO signaling pathway to cause colonic transfer dysfunction.

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Vitamin A deficiency suppresses CEACAM1 to impair colonic epithelial barrier function via downregulating microbial-derived short-chain fatty acids

Cited by 9 publications

References 47 publications

Autoinducer-2 promotes the colonization of Lactobacillus rhamnosus GG to improve the intestinal barrier function in a neonatal mouse model of antibiotic-induced intestinal dysbiosis

Autoinducer-2 promotes the colonization of Lactobacillus rhamnosus GG to improve the intestinal barrier function in a neonatal mouse model of antibiotic-induced intestinal dysbiosis

Gut microbiome: decision-makers in the microenvironment of colorectal cancer

Vitamin A deficiency triggers colonic methylation potentially impairing colonic neuron via downregulation SGK1/FOXO pathway

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