Emory_Pediatric_Strains_1
Ontology highlight
ABSTRACT:
ORGANISM(S): Helicobacter pylori
PROVIDER: GSE13317 | GEO | 2009/11/05
SECONDARY ACCESSION(S): PRJNA109905
REPOSITORIES: GEO
Similar Datasets
Project description:Array CGH analysis of Helicobacter pylori strains isolated from a North American cohort of symptomatic pediatric patients. Keywords: genotyping_design A genotyping experiment design type classifies an individual or group of individuals on the basis of alleles, haplotypes, SNP's. Patients enrolled under Benjamin Gold's Emory IRB protocol. Initial strain isolation from antral biopsies performed at Emory and culture sweeps sent to FHCRC (Seattle) for analysis. Single colony isolates (4) from each patient antral biopsy were isolated and profiled using RAPD. A single clone of each RAPD type detected in each patient (1-2) were analyzed on duplicate arrays. For analysis 500 ng of genomic DNA of each test strain was labeled with Cy5 and 500 ng of genomic DNA of a reference sample (equimolar mix of 26695 and J99) was labeled with Cy3. Strains identified as Em-patient#-clone#.
2009-11-04 | E-GEOD-13317 | biostudies-arrayexpress
Project description:Helicobacter pylori strains USU101 was infected into macaques, some of which were treated with the dietary carcinogen ENNG. After 5 years, H. pylori isolates were obtained by endoscopy followed by culture. The resulting strains were analyzed for differences in gene content by array CGH.
2014-08-18 | GSE60405 | GEO
Project description:Helicobacter pylori strains USU101 was infected into macaques, some of which were treated with the dietary carcinogen ENNG. After 5 years, H. pylori isolates were obtained by endoscopy followed by culture. The resulting strains were analyzed for differences in gene content by array CGH. Array CGH was performed by two color microarray. The monkey output strains were labeled with Cy5 (channel 2) and the input strain USU101 was labeled with Cy3 (channel 1). Each output strain was analyzed by 2-3 separate array experiments.
2014-08-18 | E-GEOD-60405 | biostudies-arrayexpress
Project description:Helicobacter pylori genome is rich in restriction - modification (R-M) systems. Around 4 % of the genome codes for components of R-M systems. hpyAVIBM, which codes for a putative phase-variable C5 - cytosine methyltransferase (MTase) from H. pylori lacks a cognate restriction enzyme. To analysis the effect of deleting hpyAVIBM on the Helicobacter pylori transcriptome, microarray analysis was done with the wild type strains and corresponding hpyAVIBM deletion strains
2011-03-16 | E-GEOD-27946 | biostudies-arrayexpress
Project description:The monkey infecting Helicobacter pylori strain USU101 used in a long term infection of macaques with and without the dietary carcinogen ENNG was analyzed for gene content compared to the sequenced strains 26695 and J99 We performed array CGH using two microarrays to analyze the gene content of the starting strain (USU101) used for the monkey infection experiment (GSE60405). The ENNG information is not relevant.
2014-08-18 | E-GEOD-60404 | biostudies-arrayexpress
Project description:Carcinogenic bacteria, Helicobacter pylori, induce DNA double-strand breaks in infected host cells. Therefore, we have investigated which genes are upregulated after the infection. Although Helicobacter pylori infection is etiologically related to the inflammation-related malignancy, gastric cancers, it role in the molecular pathogenesis of disease remains unclear. In vitro studies have suggested the infection may cause breaks in double-stranded DNA. We used microarray analysis of H. pylori-infected human gastric biopsies to investigate the effect of H. pylori on gene expression genes involved in DNA repair and DNA damage response. Micro-array analysis and immunohistochemistory showed that ATM (ataxia-telangiectasia mutated) was upregulated in H. pylori gastritis but down regulated in the premalignant lesion, intestinal metaplasia. Studies in gastric cancer cell lines showed that H. pylori-infection induced activation of ATM and formation of γ-H2AX. γ-H2AX formation was present following infection with bout cag pathogenicity island (PAI)- positive and negative strains but more robust with cag PAI positive strains consistent with the fact that both cag PAI positive negative strains are associated with gastric cancer but the risk is higher with cag PAI positive strains. Eradication of H. pylori infection is associated with a reduction in cancer risk even in the most high risk populations. These data provide a plausible molecular mechanism for a direct bacterial-host interaction increasing cancer risk.
2014-08-23 | GSE60661 | GEO
Project description:Carcinogenic bacteria, Helicobacter pylori, induce DNA double-strand breaks in infected host cells, while ATM-dependent DNA damage responses in host cells suppress genome instabilities caused by DNA breakages, which resulting in the suppression of H. pylori-induced gastric cancers. Although Helicobacter pylori infection is etiologically related to the inflammation-related malignancy, gastric cancers, it role in the molecular pathogenesis of disease remains unclear. In vitro studies have suggested the infection may cause breaks in double-stranded DNA. We used microarray analysis of H. pylori-infected human gastric biopsies to investigate the effect of H. pylori on gene expression genes involved in DNA repair and DNA damage response. Micro-array analysis and immunohistochemistory showed that ATM (ataxia-telangiectasia mutated) was upregulated in H. pylori gastritis but down regulated in the premalignant lesion, intestinal metaplasia. Studies in gastric cancer cell lines showed that H. pylori-infection induced activation of ATM and formation of γ-H2AX. γ-H2AX formation was present following infection with bout cag pathogenicity island (PAI)- positive and negative strains but more robust with cag PAI positive strains consistent with the fact that both cag PAI positive negative strains are associated with gastric cancer but the risk is higher with cag PAI positive strains. Eradication of H. pylori infection is associated with a reduction in cancer risk even in the most high risk populations. These data provide a plausible molecular mechanism for a direct bacterial-host interaction increasing cancer risk.
2014-08-23 | GSE60662 | GEO
Project description:The monkey infecting Helicobacter pylori strain USU101 used in a long term infection of macaques with and without the dietary carcinogen ENNG was analyzed for gene content compared to the sequenced strains 26695 and J99
2014-08-18 | GSE60404 | GEO
Project description:Helicobacter pylori, which is known as pathogens of various gastric diseases, have many types of genome sequence variants. That is part of the reason why pathogenesis and infection mechanisms of the H. pylori-driven gastric diseases have not been well clarified yet. Here we performed a large-scale proteome analysis to profile the heterogeneity of the proteome expression of 7 H. pylori strains by using LC/MS/MS-based proteomics approach combined with a customized database consisting of non-redundant tryptic peptide sequences derived from full genome sequences of 52 H. pylori strains. The non-redundant peptide database enabled us to identify more peptides in the database search of MS/MS data, compared with a simply merged protein database. Using the approach we performed proteome analysis of genome-unknown strains of H. pylori in as large-scale as genome-known ones. Clustering of the H. pylori strains using the proteome profiling slightly differed from the genome profiling and more clearly divided the strains into two groups based on the isolated area. Furthermore, we also identified phosphorylated proteins and sites of the H. pylori strains and obtained phosphorylation motif located in the N-terminus, which are commonly observed in bacteria.
2018-12-28 | PXD011364 | JPOST Repository
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