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16S V3-V4 -based microbial profiling of matched healthy and inflamed ileal mucosa from patients affected by Crohn’s disease (set 2)

ABSTRACT: 16S V3-V4 -based microbial profiling of matched healthy and inflamed ileal mucosa from patients affected by Crohn’s disease (set 2)

PROVIDER: PRJNA814642 | ENA |

REPOSITORIES: ENA

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16S V3-V4 -based microbial profiling of matched healthy and inflamed ileal mucosa from patients affected by Crohn’s disease

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Project description:16S V3-V4 -based microbial profiling of matched healthy and inflamed ileal mucosa from patients affected by Crohn’s disease

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Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [16S rRNA]

Project description:Crohn’s disease is a chronic, debilitating inflammatory bowel disease. Here we report a critical role for phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3- deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was due to PLC-3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/-catenin signaling, which is essential for homeostasis and regeneration of the intestinal epithelium. PLC-β3 regulated the Wnt/β-catenin pathway in small intestinal epithelial cells (IECs) at transcriptional, epigenetic, and potentially protein-protein interaction levels. PLC-β3- deficient IECs were unable to respond to stimulation by R-spondin 1, an enhancer of Wnt/β-catenin signaling. Reduced expression of PLC-β3 and its signature genes was found in biopsies of ileal Crohn’s disease patients. PLC-β regulation of Wnt signaling was evolutionally conserved in Drosophila. Our data indicate that reduction of PLC-β3- mediated Wnt/β-catenin signaling contributes to the pathogenesis of ileal Crohn’s disease.

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Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [ATAC-Seq]

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