Expression data from Helicobacter pylori-infected mouse gastric epithelial progenitor and non-progenitor cells.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE10262 | GEO | 2008/02/22
SECONDARY ACCESSION(S): PRJNA108457
REPOSITORIES: GEO
Similar Datasets
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 and Kx2 were also grown in cell media in the absence of cells. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array
2008-02-22 | GSE10261 | GEO
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) and non-progenitor gastric epithelial cells (npGECs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Experiment Overall Design: mGEPs and npGECs were seeded and grown to 70% confluency in RPMI1640 medium supplemented with 10% FBS before being infected with H. pylori strains Kx1 or Kx2 that had been grown to log phase. After 24h, media and non-attached bacteria were washed off and the cells harvested by trypsinization. RNA was prepared from triplicate cultures of mGEP cells infected with Kx1 or Kx2, npGECs infected with Kx1 or Kx2 and uninfected mGEPs and npGECs that served as controls.
2008-04-07 | E-GEOD-10262 | biostudies-arrayexpress
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 and Kx2 were also grown in cell media in the absence of cells. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array H. pylori strains Kx1 or Kx2 that had been grown to log phase were used to infect mGEP cells.. After 24h, media and non-attached bacteria were washed off and the cells harvested by trypsinization. RNA was prepared from bacteria infecting mGEP cells or bacterial cultures of Kx1 and Kx2 grown in cell media for 24h in the absence of mGEP cells.
2010-05-26 | E-GEOD-10261 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE16390: Response of gastric epithelial progenitors to H. pylori isolates from Swedish patients with chronic atrophic gastritis 1 GSE16439: Response of gastric epithelial progenitors to H. pylori isolates from Swedish patients with chronic atrophic gastritis 2 Refer to individual Series
2009-10-26 | E-GEOD-16440 | biostudies-arrayexpress
Project description:Helicobacter pylori colonization of the human stomach is a strong risk factor for gastric cancer. To investigate H. pylori-induced gastric molecular alterations, we used a Mongolian gerbil model of gastric carcinogenesis. Histologic evaluation revealed varying levels of atrophic gastritis (a premalignant condition characterized by parietal and chief cell loss) in H. pylori-infected animals, and transcriptional profiling revealed a loss of markers for these cell types. We then assessed the spatial distribution and relative abundance of proteins in the gastric tissues using imaging mass spectrometry and liquid chromatography with tandem mass spectrometry (LC-MS/MS). We detected striking differences in protein content of corpus and antrum tissues. 492 proteins were preferentially localized to the corpus in uninfected animals. The abundance of 91 of these proteins was reduced in H. pylori-infected corpus tissues exhibiting atrophic gastritis compared to infected corpus tissues with non-atrophic gastritis or uninfected corpus tissues; these included numerous proteins with metabolic functions. Fifty proteins localized to the corpus in uninfected animals were diffusely delocalized throughout the stomach in infected tissues with atrophic gastritis; these included numerous proteins with roles in protein processing. Corresponding alterations were not detected in animals infected with a H. pylori ∆cagT mutant (lacking Cag type IV secretion system activity). These results indicate that H. pylori can cause loss of proteins normally localized to the gastric corpus as well as diffuse delocalization of corpus-specific proteins, resulting in marked changes in the normal gastric molecular partitioning into distinct corpus and antrum regions.
2023-12-04 | PXD046333 | Pride
Project description:Helicobacter pylori (H. pylori) is a human pathogen that infects almost half of the world’s population. Infection with H. pylori is frequently associated with chronic gastritis and can even lead to gastric and duodenal ulcers and gastric cancer. Although the persistent colonization of H. pylori and the development of H. pylori-associated gastritis remain poorly understood, it is believed that, in gastric mucosa, the modulated gastric epithelial cells (GECs) by H. pylori are key contributors. We used microarrays to detail the global programme of gene expression in Helicobacter pylori infected-gastric epithelial cell line AGS cells and identified up-regulated genes induced by Helicobacter pylori infection.
2024-04-18 | GSE264263 | GEO
Project description:Chronic infection with the bacterial pathogen Helicobacter pylori is a risk factor for the development of gastric cancer, yet remains asymptomatic in a majority of individuals. We report here that the C57Bl6 mouse model of experimental infection with the closely related H. felis recapitulates this wide range in host susceptibility. A majority of infected mice develop premalignant lesions such as gastric atrophy, compensatory epithelial hyperplasia and intestinal metaplasia, whereas a minority is completely protected from preneoplasia. Protection is associated with the failure to mount an IFN-gamma response to the infection and an associated high Helicobacter burden. We demonstrate that IFN-gamma is essential for clearance of Helicobacter, but also mediates the formation of preneoplastic lesions. We further provide evidence that IFN-gamma triggers a specific transcriptional program in murine gastric epithelial cells in vitro and in vivo, and induces their preferential transformation to the hyperplastic phenotype. In summary, our data suggest a dual role for IFN-gamma in Helicobacter pathogenesis that could provide an explanation for the differential susceptibility to H. pylori-induced gastric pathology in the human population. Keywords: response to in vitro stimulus / comparison of histopathological states We chose mice for gene expression profiling that following Helicobacter infection had (a) symptoms of gastritis, but no epithelial changes, (b) atrophic gastritis accompanied by corpus gland hyperplasia or (c) atrophic gastritis accompanied by intestinal metaplasia. An uninfected control group was also included in the analysis, as were two groups of mice that lacked mature T- and B-cells due to a deletion mutation in the rag1 gene (Rag-1-/-) and that were either experimentally infected or served as Rag-1-/- uninfected controls. To see the effects of IFNg on murine gastric epithelial cells we analysed an immortalized murine primary gastric epithelial cell line treated with three different concentrations of IFNg in comparison to an untreated control.
2009-03-05 | E-GEOD-13873 | biostudies-arrayexpress
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:It is well-known that atrophic gastritis is a major risk factor for gastric cancer, which leads to variations in the serum levels of gastrin, pepsinogen (PG) I, and PGII. We want to assess the effects of age, sex, and Helicobacter pylori status on pepsinogen (PG) level for atrophic gastritis and whether gastric atrophy based on the PG test would be improved after H. pylori eradication.
| 2170156 | ecrin-mdr-crc
Project description:Gastric cancer is an important health problem because it is difficult to diagnose and treat in advanced stage. This makes that the prognosis of gastric cancer patients remains scarce. Currently it is known that the cause of gastric cancer is attributed to chronic infection with Helicobacter pylori. Its persistent infection leads to development of chronic atrophic gastritis that is considered as a predecessor stage of intestinal-type gastric cancer. The understanding of the alteration of molecular mechanisms during the early stages of the development of gastric cancer, and the identification of their potential biomarkers can allow a rapid diagnosis that leads to an improvement diagnosis and increase the patient’s prognosis. We analyzed gene expression profiles of patients with chronic atrophic gastritis and gastric cancer through microarray analysis, functional enrichment analysis and validation of gene expression by quantitative PCR. Gene expression profiles in patients with chronic atrophic gastritis showed molecular changes of the gastric mucosa, which leads to intestinal metaplasia and subsequently, gastric cancer. In gastric cancer the gene expression profile showed the stage of tumor progression, the product of these genes are potential biomarkers of early stages of cancer that can be potential therapeutic targets. Accordingly, the transcriptome analysis revealed several gene groups are related to development of chronic atrophic gastritis, some of which were inhibited in gastric cancer patients. The increased expression of CLDN1, CLDN7, OLFM4, c-Myc and MMP-9 genes in chronic atrophic gastritis and gastric cancer point outs to their use as promising biomarkers for the early diagnosis of gastric cancer.
2019-12-18 | GSE116312 | GEO