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DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE184314 | GEO | 2023/09/01

REPOSITORIES: GEO

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DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing [BiSulfite-seq]

Project description:A genome-wide DNA methylation study was conducted using base resolution bisulfite sequencing for purified intestinal CD4+ cells (resected or biopsied mucosa of a terminal ileum) from 21 patients with Crohn’s disease and 12 age/sex matched controls. The sequencing data was analyzed for differentially methylated CpGs (DMCs) and differentially methylated regions (DMRs). Integration was performed with RNA-sequencing data for the same set of samples to verify the functional impact of DNA methylation changes.

2023-09-01 | GSE184312 | GEO

DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing [RNA-seq]

2023-09-01 | GSE184307 | GEO

DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing

Project description:DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing

| PRJNA763982 | ENA

DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing [BiSulfite-seq]

Project description:DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing [BiSulfite-seq]

| PRJNA763988 | ENA

DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing [RNA-seq]

Project description:DNA methylation landscape and signature of CD4+ lymphocytes of lamina propria in Crohn's patients by reduced representation and bisulfite sequencing [RNA-seq]

| PRJNA763930 | ENA

Antigen-specific effector CD4 T lymphocytes school lamina propria dendritic cells to transfer innate tolerance.

Project description:Dendritic cells (DCs) have been shown to play a major role in oral tolerance, and this function has been associated with their ability to produce anti-inflammatory cytokines and to induce suppressive regulatory T cells. In this study, we demonstrate that upon oral administration of Ag, lamina propia (LP) DCs engage specific T cells and acquire a novel mechanism by which they transfer tolerance against diverse T cell specificities. Indeed, when Ig-myelin oligodendrocyte glycoprotein (MOG) carrying the MOG(35-55) epitope was orally administered into either T cell-sufficient or -deficient mice, only the T cell-sufficient hosts yielded CD8?(+) and CD8?(-) LP DCs that were able to transfer tolerance to a variety of MHC class II-restricted effector T cells. Surprisingly, these LP DCs upregulated programmed cell death ligand 1 during the initial interaction with MOG-specific T cells and used this inhibitory molecule to suppress activation of T cells regardless of Ag specificity. Furthermore, oral Ig-MOG was able to overcome experimental autoimmune encephalomyelitis induced with CNS homogenate, indicating that the DCs are able to modulate disease involving diverse T cell specificities. This previously unrecognized attribute potentiates DCs against autoimmunity.

| S-EPMC3679289 | biostudies-literature

CD4+/IL‑4+ lymphocytes of the lamina propria and substance P promote colonic protection during acute stress.

Project description:Life stress may influence symptom onset and severity in certain gastrointestinal disorders in association with a dysregulated intestinal barrier. It has been widely accepted that stress triggers the hypothalamus‑pituitary‑adrenal (HPA) axis, releasing corticosterone, which promotes intestinal permeability. In response, colonic inflammation alters mucosal immune homeostasis and destroys the colonic architecture, leading to severe intestinal diseases. Endogenous substance P (SP) does not inhibit the initial extent of the HPA axis response to restraint stress, but it reduces the duration of the stress, suggesting that SP plays an important role in the transition between acute and chronic stress. The present study aimed to investigate the effect of two groups of mice exposed to stress, including acute and chronic stress. The corticosterone was evaluated by ELISA, colon samples were obtained to detected polymorphonuclear cells by hematoxylin and eosin staining, goblet and mast cells were identified by immunocytochemistry and cytokine‑producing CD4+ T cells were analyzed by flow cytometry assays, adhesion proteins in the colon epithelium by western blotting and serum SP levels by ELISA. The results demonstrated an increase in the number of polymorphonuclear, goblet and mast cells, a decrease in claudin‑1 expression and an elevation in E‑cadherin expression during acute stress. Increased E‑cadherin expression was also detected during chronic stress. Moreover, it was found that acute stress caused a shift towards a predominantly anti‑inflammatory immune response (T helper 2 cells), as shown by the increase in the percentage of CD4+/IL‑6+ and CD4+/IL4+ lymphocytes in the lamina propria and the increase in serum SP. In conclusion, this response promoted colonic protection during acute stress.

| S-EPMC8767552 | biostudies-literature

Deregulation of Long Intergenic Non-coding RNAs in CD4+ T Cells of Lamina Propria in Crohn's Disease Through Transcriptome Profiling.

Project description:BackgroundThe aetiology of Crohn's disease [CD] involves immune dysregulation in a genetically susceptible individual. Genome-wide association studies [GWAS] have identified 200 loci associated with CD, ulcerative colitis, or both, most of which fall within non-coding DNA regions. Long non-coding RNAs [lncRNAs] regulate gene expression by diverse mechanisms and have been associated with disease activity in inflammatory bowel disease. However, disease-associated lncRNAs have not been characterised in pathogenic immune cell populations.MethodsTerminal ileal samples were obtained from 22 CD patients and 13 controls. RNA from lamina propria CD4+ T cells was sequenced and long intergenic non-coding RNAs [lincRNAs] were detected. Overall expression patterns, differential expression [DE], and pathway and gene enrichment analyses were performed. Knockdown of novel lincRNAs XLOC_000261 and XLOC_000014 was performed. Expression of Th1 or Th17-associated transcription factors, T-bet and RORγt, respectively, was assessed by flow cytometry.ResultsA total of 6402 lincRNAs were expressed, 960 of which were novel. Unsupervised clustering and principal component analysis showed that the lincRNA expression discriminated patients from controls. A total of 1792 lincRNAs were DE, and 295 [79 novel; 216 known] mapped to 267 of 5727 DE protein-coding genes. The novel lincRNAs were enriched in inflammatory and Notch signalling pathways [p <0.05]. Furthermore, DE lincRNAs in CD patients were more frequently found in DNA regions with known inflammatory bowel disease [IBD]-associated loci. The novel lincRNA XLOC_000261 negatively regulated RORγt expression in Th17 cells.ConclusionsWe describe a novel set of DE lincRNAs in CD-associated CD4+ cells and demonstrate that novel lincRNA XLOC_000261 appears to negatively regulate RORγt protein expression in Th17 cells.

| S-EPMC6930003 | biostudies-literature

Lamina propria macrophage phenotypes in relation to Escherichia coli in Crohn's disease.

Project description:BackgroundAbnormal handling of E. coli by lamina propria (LP) macrophages may contribute to Crohn's disease (CD) pathogenesis. We aimed to determine LP macrophage phenotypes in CD, ulcerative colitis (UC) and healthy controls (HC), and in CD, to compare macrophage phenotypes according to E. coli carriage.MethodsMucosal biopsies were taken from 35 patients with CD, 9 with UC and 18 HCs. Laser capture microdissection was used to isolate E. coli-laden and unladen LP macrophages from ileal or colonic biopsies. From these macrophages, mRNA was extracted and cytokine and activation marker expression measured using RT-qPCR.ResultsE. coli-laden LP macrophages were identified commonly in mucosal biopsies from CD patients (25/35, 71 %), rarely in UC (1/9, 11 %) and not at all in healthy controls (0/18). LP macrophage cytokine mRNA expression was greater in CD and UC than healthy controls. In CD, E. coli-laden macrophages expressed high IL-10 & CD163 and lower TNFα, IL-23 & iNOS irrespective of macroscopic inflammation. In inflamed tissue, E. coli-unladen macrophages expressed high TNFα, IL-23 & iNOS and lower IL-10 & CD163. In uninflamed tissue, unladen macrophages had low cytokine mRNA expression, closer to that of healthy controls.ConclusionIn CD, intra-macrophage E. coli are commonly found and LP macrophages express characteristic cytokine mRNA profiles according to E. coli carriage. Persistence of E. coli within LP macrophages may provide a stimulus for chronic inflammation.

| S-EPMC4490755 | biostudies-literature

Synergy between intraepithelial lymphocytes and lamina propria T cells drives intestinal inflammation during infection.

Project description:Oral infection of C57BL/6 mice with Toxoplasma gondii triggers severe necrosis in the ileum within 7-10 days of infection. Lesion development is mediated by Th-1 cytokines, CD4+ T cells, and subepithelial bacterial translocation. As such, these features share similarity to Crohn's disease. Recently, we uncovered a role for intraepithelial lymphocytes (IELs) in mediating pathology after Toxoplasma infection. We show here that ?? and not ?? T-cell IELs mediate intestinal damage. By adoptive transfer of mucosal T cells into naive Rag1?/? mice, we demonstrate that IELs do not function alone to cause inflammatory lesions, but act with CD4+ T lymphocytes from the lamina propria (LP). Furthermore, recipient mice pretreated with broad-spectrum antibiotics to eliminate intestinal flora resisted intestinal disease after transfer of IELs and LP lymphocytes. Our data provide valuable new insights into the mechanisms of intestinal inflammation, findings that have important implications for understanding human inflammatory bowel disease.

| S-EPMC3196813 | biostudies-literature

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