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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.

2025-05-01 | GSE270624 | GEO

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PARP15 promotes vascular barrier integrity in inflammation

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Mannose ameliorates experimental colitis by protecting intestinal barrier integrity

Project description:Metabolite alteration has been associated with the pathogenesis of inflammatory bowel disease (IBD), including colitis. Mannose, a natural bioactive monosaccharide that is involved in metabolism and synthesis of glycoproteins, exhibits anti-inflammatory and anti-oxidative activities. We show here that the circulating level of mannose is increased in patients with IBD and mice with experimental colitis. Mannose treatment attenuates intestinal barrier damage in two mouse colitis models, dextran sodium sulfate (DSS)-induced colitis and spontaneous colitis in IL-10-deficient mice. We demonstrate that mannose treatment enhanced lysosomal integrity and limited the release of cathepsin B, preventing mitochondrial dysfunction and myosin light chain kinase (MLCK)-induced tight junction disruption in the context of intestinal epithelial damage. Mannose exerts a synergistic therapeutic effect with mesalamine on mouse colitis. Cumulatively, the results indicate that mannose supplementation may be an optional approach to the treatment of colitis and other diseases associated with intestinal barrier dysfunction. New potential therapies for inflammatory bowel disease are needed as not all patients respond to or maintain a response to conventional therapies. Here the authors report that mannose supplementation ameliorates experimental colitis in male mice, potentially via effects on intestinal epithelium lysosomal integrity.

| S-EPMC9381535 | biostudies-literature

Adaptive immunity to retroelements promotes barrier integrity [bulk_DC_KC_LC]

Project description:Adaptive immunity to retroelements promotes barrier integrity [bulk_DC_KC_LC]

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Adaptive immunity to retroelements promotes barrier integrity [bulk_whole_tissue]

Project description:Adaptive immunity to retroelements promotes barrier integrity [bulk_whole_tissue]

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Adaptive immunity to retroelements promotes barrier integrity [single_cell_CD8]

Project description:Adaptive immunity to retroelements promotes barrier integrity [single_cell_CD8]

| PRJNA1107514 | ENA

Adaptive immunity to retroelements promotes barrier integrity [bulk_CD8]

Project description:Adaptive immunity to retroelements promotes barrier integrity [bulk_CD8]

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Knob protein enhances epithelial barrier integrity and attenuates airway inflammation.

Project description:BackgroundAltered epithelial physical and functional barrier properties along with TH1/TH2 immune dysregulation are features of allergic asthma. Regulation of junction proteins to improve barrier function of airway epithelial cells has the potential for alleviation of allergic airway inflammation.ObjectiveWe sought to determine the immunomodulatory effect of knob protein of the adenoviral capsid on allergic asthma and to investigate its mechanism of action on airway epithelial junction proteins and barrier function.MethodsAirway inflammation, including junction protein expression, was evaluated in allergen-challenged mice with and without treatment with knob. Human bronchial epithelial cells were exposed to knob, and its effects on expression of junction proteins and barrier integrity were determined.ResultsAdministration of knob to allergen-challenged mice suppressed airway inflammation (eosinophilia, airway hyperresponsiveness, and IL-5 levels) and prevented allergen-induced loss of airway epithelial occludin and E-cadherin expression. Additionally, knob decreased expression of TH2-promoting inflammatory mediators, specifically IL-33, by murine lung epithelial cells. At a cellular level, treatment of human bronchial epithelial cells with knob activated c-Jun N-terminal kinase, increased expression of occludin and E-cadherin, and enhanced epithelial barrier integrity.ConclusionIncreased expression of junction proteins mediated by knob leading to enhanced epithelial barrier function might mitigate the allergen-induced airway inflammatory response, including asthma.

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Tmprss2 maintains epithelial barrier integrity and transepithelial sodium transport

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