Ontology highlight
ABSTRACT:
PROVIDER: PRJNA838794 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19239529_1.fastq.gz | Fastqsanger.gz | |||
| SRR19239529_2.fastq.gz | Fastqsanger.gz | |||
| SRR19239530_1.fastq.gz | Fastqsanger.gz | |||
| SRR19239530_2.fastq.gz | Fastqsanger.gz | |||
| SRR19239531_1.fastq.gz | Fastqsanger.gz |
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Project description:Helicobacter pylori enhances the risk for ulcer disease and gastric cancer, yet only a minority of H. pylori-colonized individuals develop disease. We examined the ability of two H. pylori isolates to induce differential host responses in vivo or in vitro, and then used an H. pylori whole genome microarray to identify bacterial determinants related to pathogenesis. Gastric ulcer strain B128 induced more severe gastritis, proliferation, and apoptosis in gerbil mucosa than did duodenal ulcer strain G1.1, and gastric ulceration and atrophy occurred only in B128+ gerbils. In vitro, gerbil-passaged B128 derivatives significantly increased IL-8 secretion and apoptosis compared with G1.1 strains. DNA hybridization to the microarray identified several strain-specific differences in gene composition including a large deletion of the cag pathogenicity island in strain G1.1. Partial and complete disruption of the cag island in strain B128 attenuated induction of IL-8 in vitro and significantly decreased gastric inflammation in vivo. These results indicate that the ability of H. pylori to regulate epithelial cell responses related to inflammation depends on the presence of an intact cag pathogenicity island. Use of an H pylori whole genome microarray is an effective method to identify differences in gene content between H. pylori strains that induce distinct pathological outcomes in a rodent model of H. pylori infection.
2005-06-30 | E-SMDB-1587 | biostudies-arrayexpress
Project description:Helicobacter pylori enhances the risk for ulcer disease and gastric cancer, yet only a minority of H. pylori-colonized individuals develop disease. We examined the ability of two H. pylori isolates to induce differential host responses in vivo or in vitro, and then used an H. pylori whole genome microarray to identify bacterial determinants related to pathogenesis. Gastric ulcer strain B128 induced more severe gastritis, proliferation, and apoptosis in gerbil mucosa than did duodenal ulcer strain G1.1, and gastric ulceration and atrophy occurred only in B128+ gerbils. In vitro, gerbil-passaged B128 derivatives significantly increased IL-8 secretion and apoptosis compared with G1.1 strains. DNA hybridization to the microarray identified several strain-specific differences in gene composition including a large deletion of the cag pathogenicity island in strain G1.1. Partial and complete disruption of the cag island in strain B128 attenuated induction of IL-8 in vitro and significantly decreased gastric inflammation in vivo. These results indicate that the ability of H. pylori to regulate epithelial cell responses related to inflammation depends on the presence of an intact cag pathogenicity island. Use of an H pylori whole genome microarray is an effective method to identify differences in gene content between H. pylori strains that induce distinct pathological outcomes in a rodent model of H. pylori infection. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
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Project description:Helicobacter pylori enhances the risk for ulcer disease and gastric cancer, yet only a minority of H. pylori-colonized individuals develop disease. We examined the ability of two H. pylori isolates to induce differential host responses in vivo or in vitro, and then used an H. pylori whole genome microarray to identify bacterial determinants related to pathogenesis. Gastric ulcer strain B128 induced more severe gastritis, proliferation, and apoptosis in gerbil mucosa than did duodenal ulcer strain G1.1, and gastric ulceration and atrophy occurred only in B128+ gerbils. In vitro, gerbil-passaged B128 derivatives significantly increased IL-8 secretion and apoptosis compared with G1.1 strains. DNA hybridization to the microarray identified several strain-specific differences in gene composition including a large deletion of the cag pathogenicity island in strain G1.1. Partial and complete disruption of the cag island in strain B128 attenuated induction of IL-8 in vitro and significantly decreased gastric inflammation in vivo. These results indicate that the ability of H. pylori to regulate epithelial cell responses related to inflammation depends on the presence of an intact cag pathogenicity island. Use of an H pylori whole genome microarray is an effective method to identify differences in gene content between H. pylori strains that induce distinct pathological outcomes in a rodent model of H. pylori infection. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
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Project description:Helicobacter pylori, a pathogenic member of phylum Campylobacterota (formerly Epsilonproteobacteria), is recognized as the leading cause of several human gastric pathologies, including acute and chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In the last two decades, the alarming increase of the antibiotic resistance levels to first-line and even “rescue” antibiotics, especially clarithromycin, metronidazole and levofloxacin, has led to a marked decrease of the eradication rates of traditional therapies. In previous works, we have validated the essential protein HsrA as an effective therapeutic target for H. pylori infection. HsrA is an OmpR/PhoB-type orphan response regulator, unique and highly conserved in members of phylum Campylobacterota, which appears involved in a variety of crucial physiological processes. In the present work, we carried out a transcriptomic analysis in order to discern the global effects of lethal concentrations of a bactericidal HsrA inhibitor on the H. pylori physiology. Treatment with the bactericidal HsrA inhibitor significantly changed the transcript levels of 367 open reading frames (ORF), of which 212 genes appeared upregulated and 155 genes resulted in downregulation, as compared with control samples. Thus, in vivo HsrA inhibition influenced, directly or indirectly, the expression of 23% of ORFs encoded by the H. pylori 26696 genome. Among the 268 differentially expressed genes (DEGs) with defined functions, two functional categories were highly enriched with downregulated genes involved in essential physiological processes: (1) ribosome biogenesis, and (2) electron transfer and oxidative phosphorylation.
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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.
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