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Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease [Microdissected IEC]

ABSTRACT: Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease [Microdissected IEC]

PROVIDER: PRJNA667344 | ENA |

REPOSITORIES: ENA

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Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease [Microdissected IEC]

Project description:Background and Aims: The pathophysiology of the diarrhoea-predominant inflammatory bowel disease collagenous colitis (CC) is poorly described. Our aim was to use RNA sequencing of colonic biopsies from patients with active CC, CC in remission, refractory CC, ulcerative colitis (UC), and controls to gain insight into CC pathophysiology, identify additional genetic signatures linked to CC, and uncover targets for future therapeutic agents. Methods: We performed whole transcriptome sequencing of CC colonic samples from patients before and during treatment with the corticosteroid drug budesonide, steroid-refractory patients, UC and healthy controls (n=9-13). Bulk mucosa and laser-captured microdissected intestinal epithelial cell gene expression was functionally analyzed by gene-set enrichment and gene-set variation analyses to identify statistically significant pathways and cells, respectively, that change in CC. Leading genes and cells were validated using reverse transcription quantitative PCR and/or immunohistochemistry. Finally, we compared CC transcriptome with that from UC samples. Results: We identified an activation of the adaptive immune response to bacteria in active CC compared to that in remission that could be mediated by dendritic cells. However, a unique signature of genes related to the immune response and DNA transcription remain dysregulated after achieving remission. Budesonide-refractory CC patients fail to restore normal gene expression, which results in a transcriptomic profile close to UC. Intestinal epithelial CC cells displayed an impaired cell proliferation and increased antigen presentation. Conclusion: Our study confirmed previous findings from GWAS and immunological studies related to CC pathogenesis and describes novel genes, pathways and cells that might contribute to the pathophysiology of CC, ongoing epithelial damage, and complications associated with CC.

2021-05-03 | GSE159007 | GEO

Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease

Project description:Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease

| PRJNA667340 | ENA

Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease [Whole mucosa]

Project description:Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease [Whole mucosa]

| PRJNA667343 | ENA

Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease [Whole mucosa]

2021-05-03 | GSE159008 | GEO

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

Project description:To investigate NF-kB-driven gene expression in IEC, we performed microarray analysis from enterocytes of mice that express a constitutively active form of IKKb in intestinal epithelial cells Total RNA was prepared from enterocytes obtained from small intestines of IKKb(EE)IEC and WT littermates. Two biological replicates were performed for each experimental condition.

2011-06-09 | E-GEOD-29701 | biostudies-arrayexpress

Transcriptomic profiling of collagenous colitis identifies hallmarks of non-destructive inflammatory bowel disease

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-05-03 | GSE159010 | GEO

Expression data from colon samples from FADD IEC-KO (intestinal epithelial cell-knock out) and CASP8 IEC-KO mice in combination with different genetic mutations (Zbp1 -/-, Mlkl -/-, Ripk3 IEC-KO)

Project description:FADD-IEC KO and CASP8 IEC-KO mice spontaneously develop chronic colitis charcterized by inflammatory gene expression. We characterized the role of MLKL, RIPK3, ZBP1, in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of MLKL, RIPK3 and ZBP1 on the gene expression profile in FADD IEC-KO and/or CASP8 IEC-KO mice and detect effects on specific inflammatory genes.

2020-05-01 | GSE137281 | GEO

Expression data from ileum samples from FADD IEC-KO (intestinal epithelial cell-knock out) and CASP8 IEC-KO mice in combination with different genetic mutations (Zbp1 -/-, Mlkl -/-, Ripk3 IEC-KO)

Project description:FADD-IEC KO and CASP8 IEC-KO mice spontaneously develop chronic ileitis charcterized by inflammatory gene expression. We characterized the role of MLKL, RIPK3, ZBP1, in the upregulation of inlflammatory genes in these mice. We used microarray to study the effect of MLKL, RIPK3 and ZBP1 on the gene expression profile in FADD IEC-KO and/or CASP8 IEC-KO mice and detect effects on specific inflammatory genes.

2020-05-01 | GSE137280 | GEO

Expression profile of WT and IKKb(EE)IEC epithelial cells (IEC)

2011-06-09 | GSE29701 | GEO

Expression data from jejunum IEC deleted for both HDAC1 and HDAC2

Project description:Both HDAC1 and HDAC2 are epigenetic erasers that drive specific and redundant gene expression patterns, in part by removing acetyl groups on histones. Deletion of these Hdac in intestinal epithelial cell (IEC) in vivo alters intestinal homeostasis, dependent on the Hdac deleted and the level of expression of both. To determine the intrinsic specific IEC function of HDAC1 and HDAC2, we have performed transcriptomic and quantitative proteomic approaches on IEC-deficient for Hdac1 and Hdac2. We have defined changes in both mRNA and protein expression patterns affecting IEC differentiation. We have identified IEC Hdac1- and Hdac2-dependent common as well as specific pathways and biological processes. These findings uncover unrecognized similarities and differences between normal IEC and HDAC1/2 deleted jejunum IEC.

2020-12-31 | GSE158522 | GEO

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