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A Novel Human Gastric Primary Cell Culture System for Modeling Helicobacter Pylori Infection In Vitro

ABSTRACT: We identified specific long-term culture conditions that allow the formation of 3-dimensional human gastric spheroids, which can be differentiated by withdrawal of Wnt3A and R-spondin1 to human gastric organoids. These cultures can expand indefinitely and exhibit important characteristics of human stomach tissue. Furthermore, these 3-dimensional cultures can be transferred into 2-dimensional primary epithelial cell layers, which can be successfully infected with H. pylori and thereby provide ideal conditions to study infections in vitro.

ORGANISM(S): Homo sapiens

PROVIDER: GSE58473 | GEO | 2014/12/10

SECONDARY ACCESSION(S): PRJNA252707

REPOSITORIES: GEO

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A Novel Human Gastric Primary Cell Culture System for Modeling Helicobacter Pylori Infection In Vitro

Project description:We identified specific long-term culture conditions that allow the formation of 3-dimensional human gastric spheroids, which can be differentiated by withdrawal of Wnt3A and R-spondin1 to human gastric organoids. These cultures can expand indefinitely and exhibit important characteristics of human stomach tissue. Furthermore, these 3-dimensional cultures can be transferred into 2-dimensional primary epithelial cell layers, which can be successfully infected with H. pylori and thereby provide ideal conditions to study infections in vitro. Microarray experiments were performed as dual-color hybridizations on Agilent human whole genome catalog 44K arrays. To compensate for dye-specific effects, a dye-reversal color-swap was applied.

2014-12-10 | E-GEOD-58473 | biostudies-arrayexpress

Expression data from AGS cells with Helicobacter pylori infection

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

Gene expression profiling of gastric cells infected by Helicobacter pylori

2016-03-01 | GSE70394 | GEO

Toll-like receptor 10 in Helicobacter pylori infection

Project description:Helicobacter pylori is a highly successful and important human pathogen that causes chronic gastritis, peptic ulcer diseases and gastric cancer. Innate immunity plays an important role of the primary defense against pathogens and epidemiological studies have suggested a role of toll-like receptor 1 (TLR1) in the risk of H. pylori acquisition. We performed microarray analysis of gastric mucosal biopsy specimens from H. pylori-positive and uninfected subjects; infection was associated with an ~15-fold up-regulation of TLR10 (p <0.001). Quantitative RT-PCR confirmed TLR10 mRNA levels were increased 3-fold in H. pylori-infection (p <0.001) and immunohistochemistory using anti-TLR10 polyclonal antibodies showed increased TLR10 expression in gastric epithelial cells of infected individuals. In vitro experiments where H. pylori was co-cultured with NCI-N87 gastric cells showed significant H. pylori-specific up-regulation of TLR10 mRNA levels and a correlation with TLR2 mRNA levels (R = 0.87, P <0.001). We compared combinations of TLRs for their ability to mediate NF-_B activation. NF-_B activation was increased following exposure to heat killed H. pylori or H. pylori-LPS only with the TLR2/TLR10 heterodimer. These findings suggest TLR10 is a functional receptor involved in the innate immune response to H. pylori infection and that TLR2/TLR10 heterodimer possibly functions in the recognition of H. pylori-LPS.

2015-06-01 | GSE60427 | GEO

Helicobacter pylori colonization ameliorates glucose homeostasis in mice

Project description:Background: Helicobacter pylori has been shown to alter the secretion of gastric hormones that modulate body fat deposition. Since cag-positive H. pylori strains interact intimately with the host gastric epithelial cells and trigger higher inflammation than cag-negative strains, we hypothesized that gastric colonization with H. pylori strains without functional cagA ameliorates obesity and its complications by modulating gastric gene expression and inflammation. Methodology/Principal Findings: To test this hypothesis we examined the effects of gastric colonization on metabolic and inflammatory markers in mice infected with two isogenic strains of H. pylori: 26695 strain 98-325 (cagA+ wild-type) and its cag pathogenicity island (cagPAI) mutant strain 99-305, a knockout made by inserting a chloramphenicol resistance cassette. Only the cagPAI mutant decreased fasting blood glucose levels, improved glucose tolerance and suppressed weight gain in db/db mice and mice with diet-induced obesity. These effects were associated with increased gastric leptin levels, suppressed infiltration of macrophages, enhanced influx of regulatory T cells (Treg) in adipose tissue and suppressed gastric inflammation. Gene set enrichment analyses of gastric mucosal samples identified six differentially modulated pathways, including the Hedgehog signaling pathway that is associated with control of cellular proliferation and gastric carcinogenesis as well as the insulin signaling pathway. Conclusions/Significance: Gastric colonization with cagPAI-negative strains of H. pylori ameliorate obesity and inflammation by modulating gastric gene expression, suggesting that cag-negative H. pylori strains might be beneficial in ameliorating obesity and its co-morbidities.

2010-11-13 | GSE21833 | GEO

Membrane substrates of HtrA from Helicobacter pylori

Project description:High temperature requirement A (HtrA) is a serine protease secreted by the group-I carcinogen Helicobacter pylori (H. pylori). The human cell adhesion protein and tumor suppressor E-cadherin (hCdh1) expressed on the surface of gastric epithelial cells was identified as the first HtrA substrate. HtrA-mediated hCdh1 cleavage and subsequent disruption of intercellular adhesion are considered as important steps in H. pylori pathogenesis. In this study, we performed a proteomic profiling of H. pylori HtrA (HpHtrA) to decipher the complex mechanism how H. pylori can interfere with epithelial barrier integrity.

2022-02-17 | PXD025360 | Pride

Helicobacter pylori pathogenic mechanism

Project description:Helicobacter pylori infection reprograms host gene expression and influences various cellular processes, which have been investigated by cDNA microarray in vitro culture cells and in vivo patients of the chronic abdominal complaint. In this study，the effects of H. pylori infection on host gene expression in the gastric antral mucosa of patients with chronic gastritis were examined.

2012-04-30 | GSE30042 | GEO

Gene expression profiling of gastric cells infected by Helicobacter pylori

Project description:Helicobacter pylori are gram-negative bacteria that colonize the human stomach and are the major etiological factor in gastric carcinoma development. The aim of this work was to evaluate changes in gene expression in gastric cells induced by H. pylori. The human gastric carcinoma-derived cell line AGS was infected with H. pylori strain 60190 (ATCC 49503) for 24 hours. RNA was extracted from three independent experiments.

2016-03-01 | E-GEOD-70394 | biostudies-arrayexpress

Helicobacter pylori infection dysregulates gastric proteome

Project description:The purpose of the study was to define gastric cell-specific proteomic changes, induced by H. pylori oncogenic strains, that are critical for initiation of the gastric carcinogenic cascade. Gastric cell scrapings were harvested from H. pylori-infected and uninfected animals for quantitative proteomic analyses using isobaric tags for relative and absolute quantitation (iTRAQ). Canonical and disease pathway mapping using Ingenuity Pathway Analysis (IPA) identified significantly altered inflammatory and cancer-signaling pathways that included Rab/Ras signaling proteins.

2018-11-23 | PXD009583 | Pride

Helicobacter pylori-mediated Epigenetic Dysregulation of FOXD3 Tumor-suppressive Cascade In Gastric Carcinogenesis [MMASS]

Project description:Promoter hypermethylation occurs in human gastric cancers, but whether the deregulated genes contribute to the multi-step Helicobacter pylori (H pylori)-induced gastric carcinogenesis remains unclear. We used Microarray-based Methylation Assessment of Single Samples (MMASS) to identify differential methylated genes in 10 human gastric cancer tissues.

2012-12-28 | GSE39599 | GEO

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