Ontology highlight
ABSTRACT:
PROVIDER: PRJNA606550 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11080608_1.fastq.gz | Fastqsanger.gz | |||
| SRR11080608_2.fastq.gz | Fastqsanger.gz | |||
| SRR11080609_1.fastq.gz | Fastqsanger.gz | |||
| SRR11080609_2.fastq.gz | Fastqsanger.gz | |||
| SRR11080610_1.fastq.gz | Fastqsanger.gz |
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Project description:Interleukin 27 Protects From Gastric Atrophy and Metaplasia During Chronic Autoimmune Gastritis
| PRJNA1167764 | ENA
Project description:Background & Aims: The association between chronic inflammation and gastric carcinogenesis is well established, but it is not clear how immune cells and cytokines regulate this process. We investigated the role of interleukin 27 (IL27) in the development of gastric atrophy, hyperplasia, and metaplasia (preneoplastic lesions associated with inflammation-induced gastric cancer) in mice with autoimmune gastritis. Methods: We performed studies with TxA23 mice (control mice), which express a T-cell receptor against the H+/K+ adenosine triphosphatase α chain and develop autoimmune gastritis, and TxA23xEbi3-/- mice, which develop gastritis but do not express IL27. In some experiments, mice were given high-dose tamoxifen to induce parietal cell atrophy and spasmolytic polypeptide-expressing metaplasia (SPEM). Recombinant IL27 was administered to mice with mini osmotic pumps. Stomachs were collected and analyzed by histopathology and immunofluorescence; we used flow cytometry to measure IL27 and identify immune cells that secrete IL27 in the gastric mucosa. Single-cell RNA sequencing was performed on immune cells that infiltrated stomach tissues. Results: We identified IL27-secreting macrophages and dendritic cell in the corpus of mice with chronic gastritis (TxA23 mice). Mice deficient in IL27 developed more severe gastritis, atrophy, and SPEM than control mice. Administration of recombinant IL27 significantly reduced the severity of inflammation, atrophy, and SPEM in mice with gastritis. Single-cell RNA sequencing showed that IL27 acted almost exclusively on stomach-infiltrating CD4+ T cells to suppress expression of inflammatory genes. Conclusions: In studies of mice with autoimmune gastritis, we found that IL27 is an inhibitor of gastritis and SPEM, suppressing CD4+ T-cell–mediated inflammation in the gastric mucosa.
2024-10-01 | GSE278552 | GEO
Project description:The majority of gastric cancer cases are believed to be caused by chronic infection with the bacterium Helicobacter pylori, and atrophic corpus gastritis is a predisposing condition to gastric cancer development. We aimed to increase understanding of the molecular details of atrophy by performing a global transcriptome analysis of stomach tissue. Biopsies from patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa and analyzed on microarrays. The stages included patients without current H. pylori infection, H. pylori-infected without corpus atrophy and patients with current or past H. pylori-infection with corpus-predominant atrophic gastritis.Using clustering and integrated analysis, we found firm evidence for antralization of the corpus mucosa of atrophy patients. This antralization harbored gain of gastrin expression, as well as loss of expression of corpus-related genes, such as genes associated with acid production, energy metabolism and blood clotting. The analyses provided detailed molecular evidence for simultaneous intestinal metaplasia (IM) and spasmolytic polypeptide expressing metaplasia (SPEM) in atrophic corpus tissue. Finally, acidic mammalian chitinase, a chitin-degrading enzyme produced by chief cells, was shown to be strongly down-regulated in corpus atrophy.Transcriptome analysis revealed several gene groups which are related to development of corpus atrophy, some of which were increased also in H. pylori-infected non-atrophic patients. Furthermore, loss of acidic chitinase expression is a promising marker for corpus atrophy. Biopsies from well classified patients with different stages of H. pylori infection were taken from both the antrum and corpus mucosa. These stages included H. pylori un-infected, H. pylori-infected without corpus atrophy and H. pylori-infected with corpus-predominant atrophic gastritis.
2014-02-04 | E-GEOD-27411 | biostudies-arrayexpress
Project description:Helicobacter pylori is a well-recognized bacterium associated with the development of several histopathological lesions in the stomach. The chronic infection produces an inflammatory lesion known as gastritis. This lesion can later progress to more serious lesions such as intestinal metaplasia. Some attempts in the transcriptome of these conditions have been made; these however, have yielded limited information. Given the potential of high-throughput technologies for understanding biological processes altered and in the description of biomarkers of disease, we performed a genome-wide gene expression analysis in gastric biopsies. The aim of this study was to describe the altered molecular mechanism and potential biomarkers of follicular gastritis, chronic gastritis and intestinal metaplasia, through the identification of characteristic gene expression profiles in each histopathological lesion. The exploratory set comprised twenty-one biopsies from patients with follicular gastritis (n=7), chronic gastritis (n=7), and intestinal metaplasia (n=7), which were analyzed by whole-genome gene expression microarrays. The enrichment analyses and functional annotation of genes using computational tools were performed. The bioinformatics data of the same 21 biopsies were validated by real time PCR analysis while 79 FFPE samples were analyzed by immunohistochemistry. Gene expression analyses showed profiles for each histopathological lesion. Follicular gastritis had an expression profile with marked enrichment of immunologically-related genes. In contrast, chronic gastritis was characterized by a deregulation of mitochondrial-related genes and a down regulation of genes associated with protection against oxidative stress. Meanwhile, intestinal metaplasia showed an over expression of gastrointestinal stem cell markers and molecules related to RNA metabolism. Our results provide a comprehensive and reliable gene expression analysis of follicular gastritis, chronic gastritis and intestinal metaplasia disorders. The gene expression patterns described established a clear difference between the three pathologies studied and allowed the identification of several potential biomarkers for each histological change.
2017-11-23 | GSE106656 | GEO
Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).
2020-09-01 | E-MTAB-8889 | biostudies-arrayexpress
Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).
2020-09-01 | E-MTAB-8890 | biostudies-arrayexpress
Project description:Helicobacter pylori infection can induce gastric pathologies ranging from chronic gastritis to peptic ulcers and gastric cancer. Individuals´ response to H. pylori infection is complex and it depends on a combination of environmental factors, genetic background, host response and strain virulence. The pathway towards gastric cancer is a sequence of events known as the Correa's model of gastric carcinogenesis, a stepwise inflammatory process from normal mucosa to chronic active gastritis, atrophy, metaplasia and finally gastric adenocarcinoma. This study explores gastric clinical specimens representing different steps of the Correa pathway with the aim of identifying the expression profile of coding- and non-coding RNAs (microRNAs and small RNAs) which may have a role in the Correa's model of gastric carcinogenesis and potentially develop novel clinical biomarkers. We screened for differentially expressed genes in gastric biopsies (antrum/corpus) by employing RNAseq (for microRNAs and non-coding RNAs) and microarrays (for coding RNAs).
2020-09-01 | E-MTAB-8896 | biostudies-arrayexpress
Project description:To test the hypothesis that there is a specific miRNA expression signature which characterizes Barrett's esophagus development and progression, we performed miRNA microarray analysis comparing normal esophageal squamous epithelium with the two different metaplastic lesions occuring within Barrett's mucosa (i.e. gastric metaplasia and intestinal metaplasia). Samples of H. pylori-related gastritis and gastric intestinal metaplasia were also considered in the definition of esophageal-specific miRNAs. miRNA microarray analysis was performed in a series of samples obtained from (a) 10 histologically-proven long-segment Barrett's esophagus patients; (b) 10 patients with H. pylori-related chronic atrophic gastritis. Overall, 10 normal esophageal squamous epithelium samples, 10 esophageal intestinal metaplasia samples, 10 esophageal gastric metaplasia samples, 10 H. pylori -related gastritis samples (no atrophic lesion detected; obtained from the antrum) and 10 gastric intestinal metaplasia samples (obtained from the antrum) were considered.
2011-01-01 | E-GEOD-24839 | biostudies-arrayexpress
Project description:Genome-scale DNA methylation profiling using the Infinium DNA methylation 450K BeadChip platform and samples from gastric cancer (intestinal and diffuse), precursor lesions (multifocal chronic atrophic gastritis and inestina metaplasia), non-atrophic gastritis and normal gastric mucosa.
2021-03-04 | GSE127857 | GEO
Project description:In this study we performed RNA-seq analysis of gastric corpus biopsies to study transcriptional changes during early gastric carcinogenesis. We included patients with non-atrophic gastritis, with intermediate and extensive corpus atrophy, and patients with intestinal metaplasia. We also included a control group of H. pylori-negative subjects. All subjects were from Nicaragua, which has a population of high gastric cancer risk. Total RNA samples were treated with RiboZero Magnetic (Human/Mouse/Rat) Kit (Epicentre Biotechnologies) to deplete rRNA and the cDNA libraries were prepared using ScriptSeqTM v2 RNA-Seq Library Preparation Kit (Epicentre). Sequencing was performed on the Illumina HiScan2500 platform, 2*100bp reads.
2015-12-31 | E-MTAB-3689 | biostudies-arrayexpress