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 (H. pylori) infects nearly half of the global population. H. pylori infection is associated with various gastric diseases and is a recognized causative factor for gastric cancer. The mechanisms underlying the persistent colonization of H. pylori and its role in the development and progression of gastritis-associated carcinogenesis remain unclear. To investigate the pathogenic mechanisms of H. pylori infection, we performed RNA sequencing (RNA-seq) on H. pylori-infected gastric epithelial cells and analyzed the gene expression patterns induced by H. pylori infection, aiming to provide critical insights for understanding its disease-driving pathways.
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: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:In this study, we treated the gastric cancer cell line AGS with PBS and Helicobacter pylori to perform RNA-seq analysis. A total of 18,308 different circRNA candidates were obtained in the experiment.Compared with the control, 101 significantly differentially expressed circRNAs were identified in the AGS cells infected with H. pylori, including 84 upregulated circRNAs and 17 downregulated circRNAs.Then, circMAN1A2 with the most significant expression difference was selected according to the sequencing results to study the epigenetic mechanism of H. pylori-induced gastric carcinogenesis.
