Helicobacter pylori 26695
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ABSTRACT:
PROVIDER: PRJNA79523 | ENA |
REPOSITORIES: ENA
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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: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.
2016-03-01 | GSE70394 | GEO
Project description:Transcriptome analysis of AGS cells infected with Helicobacter pylori P12
2018-09-17 | GSE73226 | GEO
Project description:Helicobacter pylori 26695 Genome sequencing
| PRJNA175543 | ENA
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
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
Project description:The HT29 derivative cell line HT29-MTX-E12 (E12) produces an adherent mucus layer predominantly of the gastric MUC5AC mucin when grown on transwells. This mucus layer supports Helicobacter pylori survival in culture. E12 cells were infected with H. pylori and the transcriptome of infected and uninfected E12 were compared. Also included for comparison was the HT29 parent cell line grown on transwells. The study focused on glycosylation related genes as these regulate the structures that have a major role to play in pathogen-host cell interaction.
2017-09-21 | GSE74492 | GEO
Project description:To distinguish between Helicobacter pylori isolates that may cause greater disease in patients, we used whole genome expression profiling as a platform to study host-pathogen interactions and identify gene signatures associated with isolates from patients with higher cancer risk.
2013-08-05 | GSE41497 | GEO
Project description:The human gastric pathogen Helicobacter pylori is extremely well adapted to the highly acidic conditions encountered in the stomach. The pronounced acid resistance of H. pylori relies mainly on the ammonia-producing enzyme urease, however, urease-independent mechanisms are likely to contribute to acid adaptation. Acid-responsive gene regulation is mediated at least in part by the ArsRS two-component system consisting of the essential OmpR-like response regulator ArsR and the non-essential cognate histidine kinase ArsS whose autophosphorylation is triggered in response to low pH. In this study by global transcriptional profiling of an ArsS-deficient H. pylori mutant grown at pH 5.0 we define the ArsR~P- dependent regulon consisting of 110 genes including the urease gene cluster, the genes encoding the aliphatic amidases AmiE and AmiF and the rocF gene encoding arginase. Transcriptome analyses were performed using a whole-genome microarray containing 1649 PCR products generated with specific primer pairs derived from the genome sequences of H. pylori 26695 (Tomb et al., 1997. The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature 388:539-547) and J99 (Alm et al., 1999. Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori. Nature 397:176-180) which were spotted in duplicate. Microarrays were produced as described by Gressmann et al. (Gressmann et al., 2005. Gain and loss of multiple genes during the evolution of Helicobacter pylori. PLoS Genet 1(4):e43). To determine genes which are differentially expressed in the ArsS-deficient mutant G27/HP165::km at pH 5.0, cDNA was prepared from RNA extracted from H. pylori G27 and G27/HP165::km after exposing the bacteria for one hour to acidic pH. A total of eight RNA samples from two independent RNA preparations from strain G27 and G27/HP165::km, respectively, was used for cDNA labelling und hybridisation. Dye reversal colour swaps were performed as follows: One cDNA sample was generated using Cy3-dCTP and the other using Cy5-dCTP resulting in four labelled cDNAs per colour swap. Cy5-dCTP and Cy3-dCTP labelled cDNAs were combined and hybridized to the H. pylori microarray. The slides were scanned using ScanArray HT and analysed by using the ScanArray express software (Perkin Elmer). Spots were flagged and eliminated from analysis when the signal to background ratio was less then three or in obvious instances of high background or stray fluorescent signals. Median intensities of spots were background corrected and differences in dye bias were normalized by using the LOWESS algorithm (Yang et al., 2002. Normalization for cDNA microarray data: a robuste composite method addressing single and multiple slide systematic variation. Nucleic Acid Res. 30:e15). The signal ratios as measure of differential expression between the red and green channels were obtained from processed signal intensities. Ratios were further analysed with Microsoft Excel (Microsoft) and SAM software for statistic significance (Tusher et al., 2001. Significance analysis of microarrays applied to the ionizing radiation response. Proc. Natl. Acad. Sci. USA 98:5116-5121). To determine the significance of differential expression RNA was isolated from the H. pylori G27 wild-type grown in BHI broth (pH 5.0), and 20 µg of this RNA were labelled either with Cy3-dCTP or with Cy5-dCTP. The two cDNA probes generated were hybridized onto the same slide, and the data were analysed as mentioned above. Signal ratios < 0.5 and > 2.0 were analyzed further.
2010-07-01 | E-GEOD-4293 | biostudies-arrayexpress
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