Helicobacter pylori 51 strain:51
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REPOSITORIES: ENA
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Project description:Helicobacter pylori, a gastroenteric pathogen believed to have co-evolved with humans for 100.000 years, has a high genetic variability that motivates the study of different H. pylori populations and the diseases caused by them in order to find determinants for disease evolution. In this study we utilized both genomic and proteomic tools to compare a H. pylori strain (Nic25_A) from Nicaragua isolated from a patient with intestinal metaplasia with the P12 strain from Europe isolated from a patient with duodenal ulcer. Differences in the protein expression levels between the two strains were determined by both label-free quantification (MaxQuant) and labelling methods (tandem mass tags, TMT), utilizing a lipid-based protein immobilization (LPI™) technique to target surface protein peptides. Using the MaxQuant software, we found 52 proteins significantly differing between the two strains (up-or-down regulated by a factor of 1.5) and with TMT we were able to find 18 proteins with different expression levels between the strains. The P12 (duodenal ulcer) strain had higher expression of genes belonging to the cagPAI operon, while Nic25_A (intestinal metaplasia) had higher expression of the acid response regulator ArsR, as well as proteins regulated by ArsR; KatA, AmiE, and proteins involved in urease production. The results show that differences in protein expression can be detected by proteomic approaches in H. pylori strains of different pathogenicity, which might have implications for studies of disease progression.
2018-10-26 | PXD005074 | Pride
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
2005-08-16 | GSE3135 | GEO
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
2005-08-16 | E-GEOD-3135 | biostudies-arrayexpress
Project description:Genome-wide association study with machine-learning between H. pylori gastric-cancer and duodenal-ulcer strain reveal discriminatory amino acid differences and novel oncoprotein candidates
| PRJDB10720 | ENA
Project description:Draft genome sequences of Helicobacter pylori isolate cultured from one patient with ulcer disease
| PRJEB1920 | ENA
Project description:Isolated from a Swedish patient with chronic atrophic gastritis
| PRJNA16183 | ENA
Project description:Causes gastric inflammation and peptic ulcer disease
| PRJNA233 | ENA
Project description:Causes gastric inflammation and peptic ulcer disease
| PRJNA234 | ENA
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. Here we describe the design and use of a high-density oligonucleotide microarray covering six sequenced H. pylori genomes as well as several sequenced plasmids. The performance of this microarray is evaluated, and its utility is illustrated for the hybridization of genomic DNA in order to compare eight uncharacterized H. pylori strains which have not been sequenced with the six known, sequenced strains. We utilize this microarray to identify variable genomic region among H. pylori strains isolated from patients with different gastroduodenal diseases in a Chinese patient population. H. pylori isolates from 2 patients with chronic superficial gastritis, 2 patients with atrophic gastritis, 2 patients with gastric ulcer, and 2 patients with gastric cancer were studied. All eight strains were isolated from Heilongjiang province of China. A number of variable regions with high genetic diversity was identified. 26 selected genes were validated by large scale PCR in both microarray tested strains while an additional 76 strains were isolated from eight provinces.
2013-11-10 | E-GEOD-32107 | biostudies-arrayexpress