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: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: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.
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 colonizes the stomach of half of the world's population, causing a wide spectrum of disease ranging from asymptomatic gastritis to ulcers to gastric cancer. Although the basis for these diverse clinical outcomes is not understood, more severe disease is associated with strains harboring a pathogenicity island. To characterize the genetic diversity of more and less virulent strains, we examined the genomic content of 15 H. pylori clinical isolates by using a whole genome H. pylori DNA microarray. We found that a full 22% of H. pylori genes are dispensable in one or more strains, thus defining a minimal functional core of 1281 H. pylori genes. While the core genes encode most metabolic and cellular processes, the strain-specific genes include genes unique to H. pylori, restriction modification genes, transposases, and genes encoding cell surface proteins, which may aid the bacteria under specific circumstances during their long-term infection of genetically diverse hosts. We observed distinct patterns of the strain-specific gene distribution along the chromosome, which may result from different mechanisms of gene acquisition and loss. Among the strain-specific genes, we have found a class of candidate virulence genes identified by their coinheritance with the pathogenicity island. Keywords: other
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, which is known as pathogens of various gastric diseases, have many types of genome sequence variants. That is part of the reason why pathogenesis and infection mechanisms of the H. pylori-driven gastric diseases have not been well clarified yet. Here we performed a large-scale proteome analysis to profile the heterogeneity of the proteome expression of 7 H. pylori strains by using LC/MS/MS-based proteomics approach combined with a customized database consisting of non-redundant tryptic peptide sequences derived from full genome sequences of 52 H. pylori strains. The non-redundant peptide database enabled us to identify more peptides in the database search of MS/MS data, compared with a simply merged protein database. Using the approach we performed proteome analysis of genome-unknown strains of H. pylori in as large-scale as genome-known ones. Clustering of the H. pylori strains using the proteome profiling slightly differed from the genome profiling and more clearly divided the strains into two groups based on the isolated area. Furthermore, we also identified phosphorylated proteins and sites of the H. pylori strains and obtained phosphorylation motif located in the N-terminus, which are commonly observed in bacteria.
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.