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.
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.
Project description:Helicobacter pylori causes chronic gastritis and avoids elimination by the immune system of the infected host. The commensal bacterium Lactobacillus acidophilus has been reported to exert beneficial effects as a supplement during H. pylori eradication therapy. In the present study, we applied whole genome microarray analysis to compare the immune response induced in murine bone marrow derived macrophages (BMDM) stimulated with L. acidophilus, H. pylori, or with both bacteria in combination Microarray expression profiling was performed to analyze stimulation of bone marrow derived macrophages with Helicobacter pylori 251, Lactobacillus acidophilus NCFM or Lactobacillus acidophilus NCFM co-stimulated with Helicobacter pylori 251 were analyzed 5 hours after infection.
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.
Project description:The purpose of this study was to examine macrophage proteomic changes induced by Helicobacter pylori. Macrophages utilized were the RAW 264.7 murine cell line. Macrophages were treated with H. pylori for 24 hours. The experimental design was a 4-plex isobaric tags for relative and absolute quantification (iTRAQ). In addition to uninfected control and H. pylori infected, the additional two conditions included an inhibitor of deoxyhypusine synthase (N1-guanyl-1,7-diamine-heptane, 1-(7-ammonioheptyl)guanidinium sulfate; GC7) an enzyme involved in the hypusination translation pathway, and the inhibitor plus H. pylori.
Project description:Based on preliminary data demonstrating that macrophages are critical regulators of Helicobacter pylori colonization and gastric pathology in mice, we sought to investigate how macrophages may serve as bacterial reservoirs of intracellular H. pylori.
Project description:Helicobacter pylori causes chronic gastritis and avoids elimination by the immune system of the infected host. The commensal bacterium Lactobacillus acidophilus has been reported to exert beneficial effects as a supplement during H. pylori eradication therapy. In the present study, we applied whole genome microarray analysis to compare the immune response induced in murine bone marrow derived macrophages (BMDM) stimulated with L. acidophilus, H. pylori, or with both bacteria in combination
Project description:Thiele2005 - Genome-scale metabolic network
of Helicobacter pylori (iIT341)
This model is described in the article:
Expanded metabolic
reconstruction of Helicobacter pylori (iIT341 GSM/GPR): an in
silico genome-scale characterization of single- and
double-deletion mutants.
Thiele I, Vo TD, Price ND, Palsson
BØ.
J. Bacteriol. 2005 Aug; 187(16):
5818-5830
Abstract:
Helicobacter pylori is a human gastric pathogen infecting
almost half of the world population. Herein, we present an
updated version of the metabolic reconstruction of H. pylori
strain 26695 based on the revised genome annotation and new
experimental data. This reconstruction, iIT341 GSM/GPR,
represents a detailed review of the current literature about H.
pylori as it integrates biochemical and genomic data in a
comprehensive framework. In total, it accounts for 341
metabolic genes, 476 intracellular reactions, 78 exchange
reactions, and 485 metabolites. Novel features of iIT341
GSM/GPR include (i) gene-protein-reaction associations, (ii)
elementally and charge-balanced reactions, (iii) more accurate
descriptions of isoprenoid and lipopolysaccharide metabolism,
and (iv) quantitative assessments of the supporting data for
each reaction. This metabolic reconstruction was used to carry
out in silico deletion studies to identify essential and
conditionally essential genes in H. pylori. A total of 128
essential and 75 conditionally essential metabolic genes were
identified. Predicted growth phenotypes of single knockouts
were validated using published experimental data. In addition,
in silico double-deletion studies identified a total of 47
synthetic lethal mutants involving 67 different metabolic genes
in rich medium.
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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