H. pylori 26695: wild-type vs nitro-oxide (NO) treated; knockout-crdS in H. pylori 26695 vs knockout-crdS with NO treatment
Ontology highlight
ABSTRACT: There are two transcription profiles. The first profiling is comparing control untreated H. pylori with H. pylori with NO treatment. And the second profiling is comparing knockout-crdS in H. pylori untreated with knockout-crdS with NO treatment. The goal was determine the effects of NO-responsive gene and crdS-regulated genes on H. pylori gene expression. Four-condition experiment, wild-type H. pylori untreated (WT –NO), H. pylori with NO treatment (WT +NO), knockout-crdS in H. pylori untreated (ΔcrdS -NO), ΔcrdS with NO treatment (ΔcrdS +NO)
Project description:There are two transcription profiles. The first profiling is comparing control untreated H. pylori with H. pylori with NO treatment. And the second profiling is comparing knockout-crdS in H. pylori untreated with knockout-crdS with NO treatment. The goal was determine the effects of NO-responsive gene and crdS-regulated genes on H. pylori gene expression.
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:This study set out to identify global changes in gene expression in MKN45 gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point.
Project description:This study set out to identify global changes in gene expression in AGS gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point.
Project description:This study set out to identify global changes in gene expression in AGS gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point. Total RNA was harvested from AGS cells following treatment with LPS for 8h or untreated cells at the same time-point. 2 independent experiments were carried out. RNA was labelled and hybridized to GeneChips to analyse changes in gene expression.
Project description:This study set out to identify global changes in gene expression in MKN45 gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point. Total RNA was harvested from MKN45 cells following treatment with LPS for 8h or untreated cells at the same time-point. 2 independent experiments were carried out. RNA was labeled and hybridized to GeneChips to analyse changes in gene expression.
Project description:Forkhead box (Fox) proteins constitute an evolutionarily conserved family of transcriptional regulators whose deregulations lead to tumorigenesis. However, their regulation and function in gastric cancer are unknown. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. FOXD3 was found to be hypermethylated in a mouse model of H pylori infection and possess tumor-suppressive functions in gastric cancer cell lines. In order to characterize the direct targets of FOXD3 that confer its actions, we performed ChIP-chip in N87 gastric cancer cell line which express low level of FOXD3 in the nuclei of a sub-population of cells. Promoter hypermethylation occurs during Helicobacter pylori (H pylori)-induced gastritis, but whether the deregulated genes contribute to the multi-step gastric carcinogenesis remains unclear. We used MethylCap-microarray to identify hypermethylated genes in a mouse model of H pylori infection. human Samples: Human gastric tumor cell line, N87 was grown in RPMI1640 supplemented with 10% fetal bovine serum. ChIP assays were performed using anti-FOXD3 antibody. The immunoprecipitated-FOXD3 and -IgG DNA were used to probe the Agilent human ChIP-chip arrays. mouse Samples: Two-condition experiment, H pylori-infected vs. control gastric tissues. 2 dye-swap replicates.
Project description:Many vaccination studies have revealed various degrees of protection in mouse models. However, the mechanism of protection is not fully understood. The aim of this study was to identify genes specifically expressed in H. pylori infection and prophylactic immunized mice. A prophylactic immunization with purified protein of H. pylori BabA combining with the mucosal CTA1-DD adjuvant was performed in a-1,3/4-fucosyltransferase transgenic FVB/N mice. Gene expression profile was analysed from the gastric mucosa among untreated, the infected and immunized mice. There were a set of genes were upregulated or downregulated respectively, in infected mice as compared with untreated mice. These include the adipokines released form adipose tissue, adhesion molecules and actin cytoskeletal rearragemet associated genes. In immunized mice, however, the host response was not as strong as in infected mice and significantly changed genes were completely overlapped with those in infected mice. The expression data from genechip was confirmed by quantitative real-time PCR assay. The microarray analysis suggests that genes such as actin cytoskeletal molecules and adipokines may be as potential targets of H. pylori infection. Prophylactic immunization with purified protein of H. pylori BabA combining with the mucosal CTA1-DD adjuvant could reduce bacteria colonization without induced a severe degree of inflammation. Keywords: response to treatment