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Single-cell profiling reveals Colonic CD8 Topography in IBD -hIL26 Mouse RNA-Seq

ABSTRACT: Aim: To assess the effect of IL-26 on mouse colonic tissue at steady state and in DSS-induced colitis through next-generation RNA sequencing of bulk RNA from colonic tissue. Results: We demonstrate an anti-inflammatory effect of IL-26 at both steady-state and after induction of DSS-colitis, through suppression of both cell recruitment and activation pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE148505 | GEO | 2020/08/02

REPOSITORIES: GEO

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Gut microbiota analysis in WT and Il17d-deficient mice treated with or without colitis

Project description:Microbiota dysbiosis has been reported to contribute to the pathogenesis of colitis, to demonstrate whether IL-17D protects against DSS-induced colitis through regulation of microflora, we performed 16S rRNA sequencing in feces from WT and Il17d-deficient mice. Our data indicate that Il17d deficiency results in microbiota dysibiosis in both steady state and DSS-induced colitis.

2021-05-20 | GSE165789 | GEO

Single-cell profiling reveals Colonic CD8 Topography in IBD

Project description:Aims: Single-cell transcriptomic analysis of CD8 T cells in colonic tissue in Health and Ulcerative Colitis Results: We demonstrated significant heterogeneity within the CD8 population, defined disease associated populations and traced lineage relationships between different T cell subtypes

2020-08-02 | GSE148837 | GEO

Loss of colonic primary cilia promotes inflammation and carcinogenesis

Project description:Primary cilia (PC) are important signaling hubs in cells and we explored their role in colorectal cancer (CRC) and colitis. In the colon we found PC to be mostly present on different subtypes of fibroblasts and exposure of mice to either chemically induced colitis-associated colon carcinogenesis (CAC) or dextran sodium sulfate (DSS)-induced acute colitis decreased PC numbers. We employed conditional knock-out strains for the PC essential genes, Kif3A and Ift88, to generate mice with reduced numbers of PC on colonic fibroblasts. These mice showed an increased susceptibility in the CAC model as well as in DSS-induced colitis. Secretome and immunohistochemical analyses of DSS-treated mice displayed an elevated production of the pro-inflammatory cytokine IL-6 in PC-deficient colons. An inflammatory environment diminished PC presence in primary fibroblast cultures. This was triggered by IL-6 as identified by RNAseq analysis together with blocking experiments, suggesting an activation loop between IL-6 production and PC loss. Notably, an analysis of PC presence on biopsies of patients with ulcerative colitis as well as CRC patients revealed decreased numbers of PC on colonic fibroblasts in pathological versus surrounding normal tissue. Taken together, we provide evidence that a decrease in colonic PC numbers promotes colitis and CRC.

2022-11-29 | PXD033440 | Pride

Colonic CD8 T Cell Topography in IBD revealed by Single-Cell Profiling

Project description:10x Chromium 5' single cell RNA-Seq and VDJ sequencing of colonic CD8+ T cell cell populations in health and Ulcerative Colitis in human patients.

2022-07-01 | GSE134649 | GEO

RNA-seq analysis of colonic intestinal epithelial cells (IECs) isolated from naive wild-type C57BL/6 mice, DSS-treated wild-type C57BL/6 mice, Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion

Project description:The aim of this study is to compare the transcriptomic profile of colonic intestinal epithelial cells (IECs) at steady-state, and in several models of colitis: in naive wild-type C57BL/6 mice, in wild-type C57BL/6 mice treated for 7 days with 3% dextran sodium sulfate (DSS) in drinking water, in Il10-/- C57BL/6 mice and Il10-/- C57BL/6 mice with IEC-specific Rabgef1 deletion. Colonic IECs were isolated and FACS-sorted, then subjected tu bulk RNA-seq.

2019-09-30 | E-MTAB-7315 | biostudies-arrayexpress

Anatabine ameliorates intestinal inflammation and reduces the production of pro-inflammatory factors in a dextran sulfate sodium mouse model of colitis.

Project description:Objective: In this study, we aimed to evaluate the anti-inflammatory properties of nicotine and anatabine in a dextran sulfate sodium (DSS) mouse model of ulcerative colitis (UC). Methods: C57BL/6 male mice (10 groups with 8 animals each) were orally administered nicotine at a concentration of 5 or 20 mg/kg body weight or anatabine at a concentration of 5 or 20 mg/kg body weight for a total of 21 days. Colitis was induced by oral administration of 3.5% DSS in drinking water ad libitum during days 14–21. Colonic samples were collected for transcriptomic analysis and multi-analyte profiling (MAP). Results: Oral administration of anatabine, but not nicotine, reduced the clinical symptoms of DSS-induced colitis. The result of gene expression analysis suggested that anatabine had a restorative effect on global DSS-induced gene expression profiles, while nicotine only had limited effects. Accordingly, MAP findings revealed that anatabine reduced the colonic abundance of DSS-associated cytokines and increased IL‑10 abundance. Conclusions: Our results support the reduction of inflammatory effects by anatabine in the DSS mouse model of UC.

2020-11-03 | E-MTAB-8543 | biostudies-arrayexpress

Interleukin 17 B is protective in colitis by regulating colonic mononuclear phagocytes in mice [BMDM]

Project description:IL17B protected mice from dextran sodium sulfate (DSS)-induced colitis since IL17B deficiency resulted in severe DSS-induced colitis with exaggerated weight loss, shorter colon length, and elevated proinflammatory cytokine production in colon. For mechanism study, we use single cell transcriptional analyses of CD45+ immune cells in colonic lamina propria to detect the effect of IL-17B on colon LP immune cells in colitis. We found increased inflammatory macrophages infiltration in colon lamina propria after colitis induction expressing inflammatory cytokines such as S100a9, S100a8, Tnf, which was confirmed by real-time PCR and flow cytometry. Reconstitute of Il17b-/- mice with recombinant IL17B alleviated the severity of DSS-induced colitis. IL17B treatment also inhibited LPS-induced inflammation in bone marrow derived macrophage and in mice. These data indicate that IL17B exerting its inhibitory role in inflammation by regulating inflammatory macrophage response. In view of the protective effect of IL17B on DSS-induced colitis and LPS-induced inflammation, IL17B might represent a novel potential therapeutic approach to treat the inflammation.

2023-01-17 | GSE162062 | GEO

Interleukin 17 B is protective in colitis by regulating colonic mononuclear phagocytes in mice

2023-01-17 | GSE161987 | GEO

Enrichment of type I interferon signaling in colonic group 2 innate lymphoid cells in experimental colitis

Project description:Group 2 innate lymphoid cells (ILC2) are enriched in colonic tissues, but their precise role under intestinal inflammation, including inflammatory bowel disease (IBD) other than helminth infection, is poorly understood. Here, we analysed global gene expression of colonic ILC2 in healthy and colitis mice and found that type I interferon (T1IFN)-stimulated genes (ISGs) are enriched in ILC2 under DSS-induced colitis. Enhancement of T1IFN signaling in ILC2 under DSS-induced colitis were correlated to downregulation in cytokine production of ILC2, such as IL-5. Blocking T1IFN signaling during colitis resulted in exaggeration of colitis both in wild-type and Rag2-deficient mice. Collectively, these findings show the potential roles of T1IFN in ILC2 contributing to the development of colitis.

2022-09-21 | GSE212939 | GEO

Immunoregulatory actions of T cell PPAR g at the colonic mucosa

Project description:BACKGROUND: Peroxisome proliferator-activated receptor g (PPAR g) is a nuclear receptor whose activation has been shown to modulate macrophage and epithelial cell-mediated inflammation. The objective of this study was to use a systems approach for investigating the mechanism by which the deletion of PPAR g in T cells modulates the severity of dextran-sodium sulfate (DSS)-induced colitis, immune cell distribution and global gene expression. METHODS: Wild-type (WT) or PPAR g flfl; CD4 Cre+ (CD4cre) mice in a C57BL/6 background were challenged with 2.5% DSS in their drinking water for 0, 2, or 7 days. Mice were scored on disease severity both clinically and histopathologically. Flow cytometry was used to assess lymphocyte and macrophage populations in the blood, spleen, and mesenteric lymph nodes (MLN). Global gene expression in colonic mucosa was profiled using Affymetrix microarrays. RESULTS: Both disease severity and inflammation-related body weight loss were accelerated by the deficiency of PPAR g in T cells. Examination of colon histopathology revealed significantly greater epithelial erosion, leukocyte infiltration, and mucosal thickening in the CD4cre mice on day 7. CD4cre mice had more CD8+ T cells than wt mice and fewer CD4+FoxP3+ regulatory T cells (Treg) and IL10+CD4+ T cells in blood and MLN, respectively. Transcriptomic profiling revealed around 3000 genes being transcriptionally altered as a result of DSS challenge in CD4cre mice. These included up-regulated adhesion molecules on day 7 and proinflammatory cytokines interleukin-6 (IL-6) and IL-1b, and suppressor of cytokine signaling 3 (SOCS-3) mRNA expression. CONCLUSIONS: These findings suggest that T cell PPAR g down-regulates inflammation during DSS colitis by inhibiting colonic expression of inflammatory mediators and increasing MLN Treg. Colonic mucosa from wt and CD4cre mice were sampled at 0 (no DSS), 2, and 7 days of DSS-induced experimental colitis

2010-07-08 | E-GEOD-20523 | biostudies-arrayexpress

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