Helicobacter pylori
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA482300 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Macrophages are important cells involved in infections responses. They are mediators of gastritis in acute Helicobacter pylori (Hp) Infection and to identify how Hp affects macrophages response to infection we measured miRNA expression after macrophages Hp infection.
2018-02-22 | GSE98641 | GEO
Project description:The human pathogen Helicobacter pylori (Hp) colonizes the gastric epithelium as a unique niche in the stomach. Infections commonly occur in childhood and persist lifelong, leading in some cases to adenocarcinoma and MALT lymphoma. Several studies define mammalian microRNAs as key regulators of the immune system and of carcinogenesis processes. Here, we show Hp infection induces miR-155 expression in epithelial and hematopoietic cells in vitro and in vivo. This induction is mediated by at least two main bacterial virulence factors, the vacuolating toxin (VacA) and the gamma-glutamyl transpeptidase (GGT) in an LPS independent manner. Using adenylate cyclases agonists and inhibitor, we demonstrated that the miR-155 microRNA regulatory cascade in Hp infection involves the second messenger cyclic adenosine monophosphate (cAMP). Furthermore, the study showed that a knock-down of the Foxp3 transcription factor in T cells abolishes miR-155 expression. Together, these findings are the first demonstration of a direct interconnection between the regulatory T cell development factor Foxp3 and a microRNA. This study supports the link between Hp infection, regulation of cellular immunity, inflammation and cancer development.
2010-12-22 | GSE18616 | GEO
Project description:Macrophages are important cells involved in infections responses. They are mediators of gastritis in acute Helicobacter pylori (Hp) infection. After macrophages infection with Hp one of the most up-regulated protein is CD300E. To identify effects of CD300E activation in macrophages an agonistic antibody was used to activate CD300E and effects on gene expression were monitored.
2018-02-22 | GSE98639 | GEO
Project description:We performed the expression RNA-seq experiments for mRNA of gastric cancer tissue. Most of gastric cancers (GCs) are accompanied by Helicobacter pylori (HP) infection. However, a very limited fraction lacks any signs of HP infection and exhibits early-stage diffuse (ED) phenotype. Although previous genomic cohorts have identified multiple driver mutations for gastric cancers including diffuse-type histology, any driver event of GC without HP has not been elucidated. The present study aims to explore the molecular mechanism with comprehensive genomic and transcriptomic analyses by comparing EDGC with and without HP. EDGCs were classified as HP-negative based on the following criteria: 1) no antibiotic eradication history, 2) no atrophic appearance by endoscopy, 3) no atrophic appearance by histology, 4) negativity in two or more tests such as rapid urease, urease breath, serum antibody, stool antigen and serum pepsinogen tests. DNAs and RNAs were extracted from EDGCs with over 10 mm in diameter to secure sufficient amount of cancer tissues. Laser-capture microdissection was then used to reduce contamination of normal cells for further molecular assays. For transcriptome analyses, we conducted RNA-seq of 2 HP-positive and 4 HP-negative fresh frozen EDGCs obtained endoscopically
2022-03-25 | GSE129219 | GEO
Project description:In this study, we purified and characterized two types of H.pylori OMVs (standard strain NCTC11637 and clinical strain Hp-400) and analyzed the proteome using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS).
2022-02-14 | PXD025216 | Pride
Project description:Background: Helicobacter pylori (HP) infection may initiate and promote progression of gastric carcinogenesis. ONECUT2 shows promise for tumor diagnosis, prognosis, and treatment. This study explored ONECUT2's role and specific mechanism underlying HP infection-associated gastric carcinogenesis to suggest a basis for targeting ONECUT2 as a therapeutic strategy for gastric cancer (GC). Methods: Public data, single-cell RNA sequencing, spatial transcriptome analysis, RNA sequencing, GC tissue specimens, and clinical survival data were analyzed. Human GC organoids, HP infection, 3D sphere-forming, and extreme-dilution nude mouse models were constructed. Western blotting, qPCR, immunohistochemical staining, dual-luciferase reporter assays, phosphokinase microarray, and immunofluorescence were used. Results: Multidimensional data supported an association between ONECUT2, HP infection, and GC pathogenesis. HP infection upregulated ONECUT2 transcriptional activity via NFκB. In vitro and in vivo experiments demonstrated that ONECUT2 increases stemness in GC cells. ONECUT2 was also shown to inhibit PPP2R4 transcription, resulting in reduced PP2A activity, which in turn increased AKT/β-catenin phosphorylation. AKT/β-catenin phosphorylation facilitates β-catenin translocation to the nucleus, initiating transcription of downstream stemness-associated genes in GC cell. HP infection could upregulate the phosphorylation of AKT and β-catenin triggered by ONECUT2 downregulation via induction of ONECUT2. Clinical survival analysis indicated that high ONECUT2 expression might be an indicator of poor prognosis in GC. Conclusion: This study highlights a critical role played by ONECUT2 in promoting HP infection-associated GC by enhancing cell stemness through the PPP2R4/AKT/β-catenin signaling pathway. These findings suggest promising therapeutic strategies and potential therapeutic targets for GC treatment. Keywords: Helicobacter pylori; gastric cancer; prognosis; tumor stemness; ONECUT2
2024-05-16 | GSE267263 | GEO
Project description:Persistent colonization of the gastric mucosa by Helicobacter pylori (Hp) elicits chronic inflammation and aberrant epithelial cell proliferation, which increases the risk of gastric cancer. We examined the ability of microRNAs to modulate gastric cell proliferation in response to persistent Hp infection and found that epigenetic silencing of miR-210 plays a key role in gastric disease progression. Importantly, DNA methylation of the miR-210 gene was increased in Hp-positive human gastric biopsies as compared to Hp-negative controls. Moreover silencing of miR-210 in gastric epithelial cells promoted proliferation. We identified STMN1 and DIMT1 as miR-210 target genes and demonstrated that inhibition of miR-210 expression augmented cell proliferation by activating STMN1 and DIMT1. Together, our results highlight inflammation-induced epigenetic silencing of miR-210 as a mechanism of induction of chronic gastric diseases, including cancer, during Hp infection.
2014-09-04 | GSE58004 | GEO
Project description:In this study, a whole-genome CombiMatrix Custom oligonucleotide tiling microarray with 90000 probes covering six sequenced Helicobacter pylori(H. pylori) genomes was designed and utilized for comparative genomic profiling of eight unsequenced strains isolated from patients with different gastroduodenal diseases in Heilongjiang province of China. Since significant genomic variation were found among these strains, an additional 76 H. pylori stains with different clinical outcomes isolated from various provinces of China were further tested by PCR to demonstrate this distinction. We observed several highly variable regions among strains of gastritis, gastric ulceration and gastric cancer. They are involved in genes associated with bacterial type I, type II and type III R-M system as well as in a virB gene neighboring the well studied cag pathogenic island. Previous studies have reported the diverse genetic characterization of this pathogenic island, but it is conserved in the strains tested by microarray in this study. Moreover, a number of genes involved in the type IV secretion system related to DNA horizontal transfer between H. pylori strains were identified based on the comparative analysis of the strain specific genes. These findings may provide new insights for discovering biomarkers for prediction of gastric diseases.
2013-11-10 | GSE32107 | GEO
Project description:The human pathogen Helicobacter pylori (Hp) colonizes the gastric epithelium as a unique niche in the stomach. Infections commonly occur in childhood and persist lifelong, leading in some cases to adenocarcinoma and MALT lymphoma. Several studies define mammalian microRNAs as key regulators of the immune system and of carcinogenesis processes. Here, we show Hp infection induces miR-155 expression in epithelial and hematopoietic cells in vitro and in vivo. This induction is mediated by at least two main bacterial virulence factors, the vacuolating toxin (VacA) and the gamma-glutamyl transpeptidase (GGT) in an LPS independent manner. Using adenylate cyclases agonists and inhibitor, we demonstrated that the miR-155 microRNA regulatory cascade in Hp infection involves the second messenger cyclic adenosine monophosphate (cAMP). Furthermore, the study showed that a knock-down of the Foxp3 transcription factor in T cells abolishes miR-155 expression. Together, these findings are the first demonstration of a direct interconnection between the regulatory T cell development factor Foxp3 and a microRNA. This study supports the link between Hp infection, regulation of cellular immunity, inflammation and cancer development. A color-swap dye reversal experimental setting was applied. Ratio profiles comprising single hybridizations were combined in an error-weighted fashion to create ratio experiments. A two-fold change expression cut off for ratio experiments was applied together with anti-correlation of ratio profiles rendering the microarray analysis set highly significant (P-value > 0.01), robust and reproducible.
2010-12-22 | E-GEOD-18616 | biostudies-arrayexpress