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Single cell RNA-seq of CD45+ cell from DSS induced colitic

ABSTRACT: single cell RNA-seq of CD45+ cell from DSS induced colitic

PROVIDER: PRJNA1206296 | ENA |

REPOSITORIES: ENA

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single cell RNA-seq of CD45+ cell from DSS induced colitic

Project description:Objective: Inflammatory bowel disease (IBD), encompassing ulcerative colitis (UC) and Crohn’s disease (CD), represents a challenging group of chronic gastrointestinal inflammatory disorders. While trained immunity, a form of innate immune memory, has shown promise in combating infection and cancer, its role in chronic inflammatory diseases, particularly inflammatory bowel disease (IBD), remains relatively underexplored. This study aims to investigate the potential of trained immunity to ameliorate IBD. Results: BG induced trained immunity significantly ameliorates DSS-induced colitis. Mechanistically, β-glucan primed the hematopoietic compartment, leading to a profound shift in monocyte fuction. Both bone marrow transplantation from trained donors to naïve recipients and adoptive transfer of trained peripheral monocytes provided protection against DSS colitis. Notably, trained mice displayed enhanced bactericidal activity against intestinal bacterial infections. Furthermore, single-cell RNA sequencing revealed that β-glucan-induced trained immunity resulted in an expansion of reparative Cx3cr1 intestinal macrophages originating from Ly6Chi monocytes, facilitating faster recovery of the colon epithelium. Conclusion: Our findings demonstrate that β-glucan effectively induces trained immunity, leading to a multifaceted protective response against experimental colitis. These findings provide compelling evidence for the therapeutic potential of harnessing trained immunity to treat IBD and offer a novel approach to modulating intestinal inflammation and restoring gut homeostasis。

2025-07-28 | GSE285859 | GEO

Effect of cholic acid on gene expression of crypts isolated from DSS-induced colitic mice

Project description:Effect of cholic acid on gene expression of crypts isolated from DSS-induced colitic mice

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MAdCAM-1 targeting strategy can prevent colitic cancer carcinogenesis and progression via suppression of immune cell infiltration and inflammatory signals

Project description:Chronic inflammation caused by infiltrating immune cells can promote colitis-associated dysplasia/colitic cancer in ulcerative colitis (UC) by activating inflammatory cytokine signaling through the IL-6/p-STAT3 and TNFα/NF-κB pathways. Mucosal addressin cell adhesion molecule-1 (MAdCAM-1) expressed on high endothelial venules promotes the migration of immune cells from the bloodstream to the gut via interaction with α4β7 integrin expressed on the immune cells. MAdCAM-1, has therefore drawn interest as a novel therapeutic target for treating active UC. However, the role of MAdCAM-1-positive endothelial cells in immune cell infiltration in dysplasia/colitic cancers remains unclear. We evaluated the expression of MAdCAM-1, CD31, and immune cell markers (CD8, CD68, CD163, and FOXP3) in samples surgically resected from 11 UC patients with dysplasia/colitic cancer and 17 patients with sporadic colorectal cancer (SCRC), using immunohistochemical staining. We used an azoxymethane/dextran sodium sulfate mouse model (AOM/DSS mouse) to evaluate whether dysplasia/colitic cancer could be suppressed with an anti-MAdCAM-1 blocking antibody by preventing immune cell infiltration. The number of MAdCAM-1-positive vessels and infiltrating CD8+, CD68+, and CD163+ immune cells was significantly higher in dysplasia/colitic cancer than in normal, SCRC, and UC mucosa. In AOM/DSS mice, the anti-MAdCAM-1 antibody reduced the number, mean diameter, depth of tumors, Ki67 positivity, number of CD8+, CD68+, and CD163+ immune cells, and the IL-6/p-STAT3 and TNF-α/NF-κB signaling. Our results indicate that targeting MAdCAM-1 is a promising strategy for controlling not only UC severity, but also carcinogenesis and tumor progression by regulating inflammation/immune cell infiltration in patients with UC.

2023-07-10 | GSE236524 | GEO

CD45+ vs CD45- RCC proteome characterization

Project description:Exploration of proteome differences between CD45+ and CD45- cell types in renal cell carcinoma tumors and normal adjacent tissue patient samples.

2020-10-14 | PXD014370 | Pride

Effect of cholic acid on gene expression of crypts isolated from DSS-induced colitic mice

Project description:To investigate the exact mechanism of CA has on DSS-induced colitis We then performed gene expression profiling analysis using data obtained from RNA-seq of 8 samples from 2 groups

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Single-cell RNA sequencing of CD45 positive cells in spleen, bone marrow, colon and periphral blood from WT and Wnt5 DKO mice under DSS treatment

Project description:We use single-cell RNA sequencing to analyze cell composition and DEGs of CD45+ cells from spleen, BM, blood, and colon of WT and Wnt5 DKO mice under DSS treatment

2024-03-31 | GSE255409 | GEO

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Project description:Fecal samples collected on day 5 from randomly selected colitic SD rats were analyzed for gut microbiota by sequencing the V4 region of the 16S rRNA gene. The orally administered Dex-P-laden NPA2 coacervate (Dex-P/NPA2) significantly restores the diversity of gut microbiota compared with colitic SD rats in the Dex-P/PBS group and the untreated colitic rats (Control).

2021-11-06 | GSE167138 | GEO

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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.

2025-09-18 | PXD063633 | Pride

Paneth cell SIRT1 deficiency protects against DSS-induced colitis

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