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Dietary 3-Aminobenzoic Acid Enhances Intestinal Barrier Integrity and Attenuates Experimental Colitis

ABSTRACT: Dietary 3-Aminobenzoic Acid Enhances Intestinal Barrier Integrity and Attenuates Experimental Colitis

PROVIDER: PRJNA1127585 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29552046_1.fastq.gz	Fastqsanger.gz
	SRR29552046_2.fastq.gz	Fastqsanger.gz
	SRR29552047_1.fastq.gz	Fastqsanger.gz
	SRR29552047_2.fastq.gz	Fastqsanger.gz
	SRR29552048_1.fastq.gz	Fastqsanger.gz

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Dietary 3-Aminobenzoic Acid Enhances Intestinal Barrier Integrity and Attenuates Experimental Colitis

Project description:Dietary components and their metabolites produced by intestinal bacteria play a crucial role in maintaining intestinal epithelial integrity. Disrupted epithelial integrity can lead to increased permeability and chronic inflammation in the colon, known as ulcerative colitis (UC), in genetically predisposed individuals. Our data identified 3-aminobenzoic acid (3-ABA) as a key metabolite that reduces epithelial permeability and enhances barrier integrity in Caco2 cells by modulating the tight junctional regulatory pathway. Attenuated experimental colitis in mice treated with 3-ABA and decreased fecal 3-ABA in patients with UC implied the potential usefulness of 3-ABA as a novel treatment target for UC.

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Project description:Patients with ulcerative colitis (UC) have a significantly impaired intestinal barrier. Hydrogen Sulfide (H2S) is a gaseous mediator that makes notable contributions in a variety of diseases, such as reducing inflammatory response in colitis. The experimental content includes the establishment of a mouse DSS-induced colitis model, mouse colon epithelial organoids culture, H&E staining and mass spectrometry analysis. We recognized that exogenous H2S donor-GYY4137 significantly alleviated the symptoms in UC mice models and maintained Minichromosome Maintenance Complex Component 2 (MCM2) expression. CBS knockdown reduced the expression of sulfhydrated Ribosomal protein S20 (RPS20-ssh) and MCM2 in the mouse colon. Cell experiments indicated that the expression of RPS20-ssh, rather than total expression of RPS20, is responsible.

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