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 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. The gastric antral mucosa was obtained from a total of 6 untreated patients undergoing gastroscopic and pathologic confirmation of chronic superficial gastritis. Three patients infected by H. pylori and 3 patients uninfected were used to cDNA microarray experiment.
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) and non-progenitor gastric epithelial cells (npGECs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 and Kx2 were also grown in cell media in the absence of cells. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array
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 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 clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 and Kx2 were also grown in cell media in the absence of cells. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Keywords: RNA Expression Array H. pylori strains Kx1 or Kx2 that had been grown to log phase were used to infect mGEP cells.. After 24h, media and non-attached bacteria were washed off and the cells harvested by trypsinization. RNA was prepared from bacteria infecting mGEP cells or bacterial cultures of Kx1 and Kx2 grown in cell media for 24h in the absence of mGEP cells.
Project description:Macrophages are important cells involved in infections responses. They are mediators of gastritis in acute Helicobacter pylori (Hp) infection. After macrophages infection with Hp one of the most up-regulated protein is CD300E. To identify effects of CD300E activation in macrophages an agonistic antibody was used to activate CD300E and effects on gene expression were monitored.
Project description:Helicobacter pylori clinical isolates can establish themselves in gastric epithelial stem cells and this interaction may have implications for gastric tumorigenesis. Mouse gastric epithelial progenitor cells (mGEPs) and non-progenitor gastric epithelial cells (npGECs) were infected for 24hrs with Helicobacter pylori clinical isolates Kx1 and Kx2. Kx1 was isolated from a patient with chronic atrophic gastritis (ChAG) and Kx2 from the same patient 4 years later, when he progressed to gastric adenocarcinoma. Experiment Overall Design: mGEPs and npGECs were seeded and grown to 70% confluency in RPMI1640 medium supplemented with 10% FBS before being infected with H. pylori strains Kx1 or Kx2 that had been grown to log phase. After 24h, media and non-attached bacteria were washed off and the cells harvested by trypsinization. RNA was prepared from triplicate cultures of mGEP cells infected with Kx1 or Kx2, npGECs infected with Kx1 or Kx2 and uninfected mGEPs and npGECs that served as controls.