Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA145163 | ENA |
REPOSITORIES: ENA
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Project description:The aim of this study is to identify alterations induced in gastric mucosa of mice exposed to Pteridium aquilinum and/or infected with Helicobacter pylori, in order to identify genes that are induced by bracken fern exerts exacerbating effects on gastric lesions associated to the infection. Six groups of C57Bl/6 mice were be used: 1) control, 2) infected Helicobacter pylori, 3) treated with Bracken fern extract orogastrically, 4) treated with Bracken fern extract in drinking water, 5) infected Helicobacter pylori + treated with Bracken fern extract orogastrically, 6) infected Helicobacter pylori + treated with Bracken fern extract in drinking water. The infection procedure was performed using an orogastric inoculation of H.pylori (strain SS1) twice in the first week. The RNA isolation was done in triplicate (3 mice per each condition). Further evaluation of morphological alterations on gastric mucosa, proliferative index and induction of DNA strand breaks will be performed in the mice stomach exposed to Pteridium aquilinum infected or not with Helicobacter pylori. Alterations of glycosylation in gastric tissues will also evaluated.
2011-09-07 | E-GEOD-31991 | biostudies-arrayexpress
Project description:The aim of this study is to identify alterations induced in gastric mucosa of mice exposed to Pteridium aquilinum and/or infected with Helicobacter pylori, in order to identify genes that are induced by bracken fern exerts exacerbating effects on gastric lesions associated to the infection.
2011-09-08 | GSE31991 | GEO
Project description:The aim of this study is to identify alterations induced in gastric mucosa of mice infected with Helicobacter pylori, in order to identify genes that associated to the infection on gastric lesions.
2023-05-04 | GSE231337 | GEO
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.
2024-04-18 | GSE264263 | GEO
Project description:Helicobacter pylori (H. pylori) is a type of pathogen in humans that has infected nearly half of the population worldwide. Infections with H. pylori are typically associated with chronic gastritis and may even lead to gastric and duodenal ulcers and stomach cancer. While the mechanisms behind persistent colonization by H. pylori and the development of gastritis associated with it remain unclear, it is generally believed that the gastric epithelial cells (GECs) modulated by H. pylori in the gastric mucosa play a crucial role. We extensively studied the global gene expression patterns in H. pylori-infected AGS cells, a line of gastric epithelial cells, and identified genes that show increased expression upon infection with H. pylori.
2024-11-25 | GSE282738 | GEO
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.
2012-04-29 | E-GEOD-30042 | biostudies-arrayexpress
Project description:To study the miRNA expression profiles and explore the underlying roles of Helicobacter pylori (H. pylori), miR-196a/b-5p, and IFG2BP1 in the carcinogenesis of gastric mucosa.
2023-11-30 | GSE216285 | GEO
Project description:The whole-genome oligonucleotide microarray analysis gives an opportunity for studying the unidentified gene expression background of the idiopathic and H.pylori related gastric erosive alterations. Using microarrays we compared the whole genome gene expression profile of HP+ and HP- gastric erosions and normal adjacent mucosa to explain the possible role and response to HP infection and to get morphology related mRNA expression patterns. Experiment Overall Design: Total RNA was extracted from frozen gastric biopsy specimens of patients with Helicobacter pylori positive (HP+) and Helicobacter pylori negative (HP-) antrum erosions (ER+), and the corresponding, adjacent normal mucosae (ER-) and hybridized on Affymetrix HGU133 Plus 2.0 microarrays
2008-06-18 | E-GEOD-5081 | biostudies-arrayexpress
Project description:HGC-27 GC cells were stimulated with Helicobacter pylori. RNA-seq was performed to identify diffferentially-expressed gene in Hp-infected gastric cancers.
2026-05-12 | GSE316165 | GEO
Project description:Gastric cancer is the fifth most common cancer and the fifth leading cause of cancer deaths worldwide. Chronic infection by the bacterium Helicobacter pylori is the most prominent gastric cancer risk factor, but only 1-3% of infected individuals will develop gastric cancer. Cigarette smoking is another independent gastric cancer risk factor, and H. pylori-infected smokers are at a 2-11-fold increased risk of gastric cancer development, but the direct impacts of cigarette smoke on H. pylori pathogenesis remain unknown. In this study, male C57BL/6 mice were infected with H. pylori and began smoking within one week of infection. The mice were exposed to cigarette smoke (CS) five days/week for 8 weeks. CS exposure had no notable impact on gross gastric morphology or inflammatory status compared to filtered-air (FA) exposed controls in mock-infected mice. However, CS exposure significantly blunted H. pylori-induced gastric inflammatory responses, reducing gastric atrophy and pyloric metaplasia development. Despite blunting these classic pathological features of H. pylori infection, CS exposures increased DNA damage within the gastric epithelial cells and accelerated H. pylori-induced dysplasia onset in the INS-GAS gastric cancer model. These data suggest that cigarette smoking may clinically silence classic clinical symptoms of H. pylori infection but enhance the accumulation of mutations and accelerate gastric cancer initiation.
2025-01-05 | GSE274834 | GEO