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Microbiota modulation by a Human Paneth cell α-defensin fragment protects against DSS-induced colitis

ABSTRACT: Microbiota modulation by a Human Paneth cell α-defensin fragment protects against DSS-induced colitis

PROVIDER: PRJEB87824 | ENA |

REPOSITORIES: ENA

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Paneth cell SIRT1 deficiency protects against DSS-induced colitis

Project description:Paneth cells, intestine-originated innate immune-like cells, are important for maintenance of the intestinal stem cell niche, gut microbiota, and gastrointestinal barrier. Dysfunctional Paneth cells under pathological conditions are a site of origin for intestinal inflammation. However, mechanisms underlying stress-induced Paneth cell dysregulation remains unclear. We have previously reported that deletion of SIRT1 in the intestinal epithelium (SIRT1 iKO) leads to hyperaction of Paneth cells along with an increased sensitivity to Dextran sodium sulfate (DSS)-induced colitis. We recently generated a Paneth-cell specific SIRT1 KO mouse model (SIRT1 PKO). Similar to mice with SIRT1 iKO mice, SIRT1 PKO mice had increased abundance as well as hyperactivation of Paneth cells in vivo and in cultured intestinal organoids. However, in contrast to the hypersensitivity of SIRT1 iKO mice to chemical- or age-induced inflammation, SIRT1 PKO mice were protected from Dextran sodium sulfate (DSS)-colitis.

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Paneth cell SIRT1 deficiency protects against DSS-induced colitis

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Effect of IL-17R in Paneth cells after DSS challenge

Project description:Mice with Paneth cell specific genetic ablation of IL-17 receptor and their WT littermates were treated with DSS (dextran sulfate sodium). Ileum tissue was used for RNA Sequencing.

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Project description:This study aims to investigate the protein expression profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis using advanced Astral-DIA quantitative proteomics technology. A total of 12 colon tissue samples were analyzed, including 6 from healthy control mice and 6 from DSS-treated mice with induced colitis. Experimental Design Species: Mus musculus (C57BL/6 strain). Tissue Source: Colon tissues were dissected, snap-frozen in liquid nitrogen, and homogenized to extract proteins. Groups: Control Group: Healthy mice without intervention. DSS Group: Mice subjected to 2.5% DSS administration for 7 days to induce colitis, validated by histopathological assessment.

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Effect of IL-17R in Paneth cells after DSS challenge

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Dextran sulfate sodium (DSS)-induced colitis in WT and NAPRT KO mice [scWT2]

Project description:NAPRT-mediated deamidated biosynthesis of nicotinamide adenine dinucleotide (NAD), an essential electron carrier for hundreds of biochemical reactions in all living cells, mediates the diet-microbe-host NAD metabolic interaction in mice. To study the function of this metabolic pathway in vivo, we recently generated a mutant mouse strain (NAPRT KO) in which a 21-nt fragment that encodes 7 amino acids in the catalytic domain of NAPRT was deleted in all cells using the CRISPR/Cas9-mediated gene editing technology. Our data showed that NAPRT KO mice are hypersensitive to DSS-induced colitis. To better understand this hypersensitivity at the molecular level, we analyzed transcriptomes of colon tissues from DSS-treated WT and NAPRT KO mice.

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Project description:Paneth cell metaplasia (PCM) is a phenomenon in which Paneth cells, typically found in the small intestine, appear in the colonic epithelium of patients with ulcerative colitis (UC). Our study demonstrates that the PCM occurrence correlates with disease duration and active inflammation. Furthermore, we reveal that the inflammation-induced cytokine IL-22 suppresses Notch signaling, thereby promoting PCM formation in the colonic epithelium while simultaneously inducing REG3A expression in metaplastic niches. In vitro, we show that Reg3a directly enhances cell proliferation and promotes wound healing using mouse colonic organoids. In vivo, Reg3aΔIEC mice in both acute and chronic DSS-induced colitis models exhibit delayed wound healing. Additionally, studies conducted with patient-derived human colonic organoids revealed that REG3A administration stimulates cell proliferation and accelerates wound healing. These findings underscore a novel protective role of PCM-mediated REG3A in the colonic epithelium of patients with UC.

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