Helicobacter pylori
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ABSTRACT:
PROVIDER: PRJNA112243 | ENA |
REPOSITORIES: ENA
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Project description:Helicobacter pylori is a human gastric pathogen associated with gastric and duodenal ulcers as well as specific gastric cancers. It is well-evidenced that motility is essential for this pathogen to colonize human gastric tissues. We found that the H. pylori G27 HP0518 mutant showed greater motility than the parental strain, leading to increased cell adhesion and subsequent CagA translocation and NF-κB activation in AGS cells. This mutant expressed a higher molecular mass flagellin A (FlaA) than the parental wild-type strain and the complemented HP0518 mutant, which correlated with differences in motility. Deglycosylation assays indicated that the increased molecular mass of the FlaA protein expressed by the mutant was due to O-linked glycoside modifications. Electron micrographs demonstrated that expression of bundle-formed flagellin filaments in the HP0518 mutant was enhanced in comparison to the wild-type strain. Different degrees of FlaA glycosylation between H. pylori strains suggested that glycosylation could affect both virulence and persistence in vivo. In conclusion, HP0518 inactivation resulted in FlaA hyper-glycosylation leading to increased virulence and motility.
2010-12-22 | GSE14752 | GEO
Project description:Helicobacter pylori is a human gastric pathogen associated with gastric and duodenal ulcers as well as specific gastric cancers. It is well-evidenced that motility is essential for this pathogen to colonize human gastric tissues. We found that the H. pylori G27 HP0518 mutant showed greater motility than the parental strain, leading to increased cell adhesion and subsequent CagA translocation and NF-κB activation in AGS cells. This mutant expressed a higher molecular mass flagellin A (FlaA) than the parental wild-type strain and the complemented HP0518 mutant, which correlated with differences in motility. Deglycosylation assays indicated that the increased molecular mass of the FlaA protein expressed by the mutant was due to O-linked glycoside modifications. Electron micrographs demonstrated that expression of bundle-formed flagellin filaments in the HP0518 mutant was enhanced in comparison to the wild-type strain. Different degrees of FlaA glycosylation between H. pylori strains suggested that glycosylation could affect both virulence and persistence in vivo. In conclusion, HP0518 inactivation resulted in FlaA hyper-glycosylation leading to increased virulence and motility. Microarray experiments were carried out as two-color hybridizations with a color-swap dye-reversal setting to compensate Cy-dye specific effects and to ensure statistically relevant data.
2010-12-22 | E-GEOD-14752 | biostudies-arrayexpress
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 G27 Genome sequencing
| PRJNA249072 | ENA
Project description:TC1: gastric epithelial (AGS) cells infected with wild type H. pylori (G27) and isogenic mutants in cagA and vacA for 0, 0.5, 3, 6, and 12 hours. Total RNA was used to make single stranded Cy5 labelled probe and compared to Cy3 labelled probe from uninfected AGS cells. Hybridizations of G27 (trial 4) and cagA- (trial 3) timecourses were done in parallel. A technical replicate of the G27 time course (trial 5) and hybridization of vacA- (trial 3) time course were done in parallel. The cagA 6 and 12 hour time points were technically replicated (trial 4) (the cagA 6 hour sample of trial 3 was lost). TC2: Biological replication and expansion of TC1, using more isogenic mutants and timepoints. AGS cells were mock infected, infected with G27, and isogenic mutants in cagN, cagA, cagE, and a deletion of the cag PAI for 0. 1, 3, 6, 12, and 24 hours. Probe synthesis and hybridization was done as in TC1. Note: there may have been a sample mix-up with PAI 12, swapping it with G27 or cagN 12. Groups of assays that are related as part of a time series. Keywords: time_series_design
2005-11-04 | GSE3556 | GEO
Project description:Helicobacter pylori G27 Transcriptome or Gene expression
| PRJNA545152 | ENA
Project description:In this study several putative targets of the RRM protein RbpH (HPG27_786) were identified. Potential targets of RbpH in H. pylori (G27) were identified using total RNA-seq.
2020-11-25 | GSE63832 | GEO
Project description:In this study several putative targets of the RRM protein RbpH (HP0827/HPG27_786) were identified. RNA binding targets of RbpH in two strains of H. pylori (G27 and 26695) were identified using RIP-seq.
2020-11-25 | GSE63833 | GEO
Project description:TC1: gastric epithelial (AGS) cells infected with wild type H. pylori (G27) and isogenic mutants in cagA and vacA for 0, 0.5, 3, 6, and 12 hours. Total RNA was used to make single stranded Cy5 labelled probe and compared to Cy3 labelled probe from uninfected AGS cells. Hybridizations of G27 (trial 4) and cagA- (trial 3) timecourses were done in parallel. A technical replicate of the G27 time course (trial 5) and hybridization of vacA- (trial 3) time course were done in parallel. The cagA 6 and 12 hour time points were technically replicated (trial 4) (the cagA 6 hour sample of trial 3 was lost). TC2: Biological replication and expansion of TC1, using more isogenic mutants and timepoints. AGS cells were mock infected, infected with G27, and isogenic mutants in cagN, cagA, cagE, and a deletion of the cag PAI for 0. 1, 3, 6, 12, and 24 hours. Probe synthesis and hybridization was done as in TC1. Note: there may have been a sample mix-up with PAI 12, swapping it with G27 or cagN 12. Groups of assays that are related as part of a time series. Computed
2005-11-03 | E-GEOD-3556 | biostudies-arrayexpress
Project description:Chronic infection of the human stomach with Helicobacter pylori leads to a variety of pathologic sequelae including peptic ulcer and gastric cancer, resulting in significant human morbidity and mortality. Several genes have been implicated in disease related to H. pylori infection including the vacuolating cytotoxin and the cag pathogenicity island. Other factors important for establishment and maintenance of infection include urease enzyme production, motility, iron uptake and stress response. We utilized a C57BL/6 mouse infection model to query a collection of 2400 transposon mutants in two different bacterial strain backgrounds for H. pylori genetic loci contributing to colonization of the stomach. Microarray based tracking of transposon mutants allowed us to monitor the behavior of transposon insertions in 758 different gene loci. Of the loci measured 223 (29%) had a predicted colonization defect. These include previously described H. pylori virulence genes, genes implicated in virulence in other pathogenic bacteria and 81 hypothetical proteins. We have retested 10 previously uncharacterized candidate colonization gene loci by making independent null alleles and confirmed their colonization phenotype using competition experiments and determination of the dose required for 50% infection. Of the genetic loci retested, 60% have strain specific colonization defects while 40% had phenotypes in both strain backgrounds for infection, highlighting the profound effect of H. pylori strain variation on the pathogenic potential of this organism. This SuperSeries is composed of the SubSeries listed below.
2006-12-15 | GSE6531 | GEO