Mus musculus
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ABSTRACT:
PROVIDER: PRJNA96295 | ENA |
REPOSITORIES: ENA
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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 The gastric antrum form three groups of mice were prepared for Affymetrix gene chip analysis, using samples from the infected group, untreated control group (not immunized and not challenged) and the immunized group (challenged J99 four weeks after immunization). Four mice in each group were analysis by microarray.
2011-01-04 | E-GEOD-5398 | biostudies-arrayexpress
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
2011-01-04 | GSE5398 | GEO
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 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) infection is associated with an inflammatory response in the gastric mucosa, ultimately leading to cellular hyperproliferation and malignant transformation. Hitherto, only expression of a single gene, or a limited number of genes, has been investigated in infected patients. Thus, the impact of H. pylori on the expression of a broad set of genes has not yet been analyzed. cDNA arrays were therefore used to establish the global pattern of gene expression in gastric tissue of healthy subjects and of H. pylori infected patients. Two main gene expression profiles were identified based on cluster analysis. The data obtained suggest a strong involvement of selected Toll-like receptors (TLRs)3, adhesion molecules, chemokines, and interleukins in the mucosal response. This pattern is clearly different from that observed using gastric epithelial cell lines infected in vitro with H. pylori. The genotype of the bacteria (presence of genes encoding CagA, VacA and BabA) was analyzed by PCR and shown to be associated with different expression profiles. The presence of a Keywords = H. pylori Keywords = gastric inflammation Keywords = cytokines Keywords: parallel sample
2004-01-07 | GSE581 | GEO
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:We are investigating the mRNA expression profiles of gastric tissue within H. pylori-infected mice treated with estradiol, tamoxifen, or placebo We used microarrays to compare the global mRNA expression profiles in H. pylori infected mice in response to estradiol and tamoxifen
2011-06-30 | GSE29715 | 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:Background: Helicobacter pylori has been shown to alter the secretion of gastric hormones that modulate body fat deposition. Since cag-positive H. pylori strains interact intimately with the host gastric epithelial cells and trigger higher inflammation than cag-negative strains, we hypothesized that gastric colonization with H. pylori strains without functional cagA ameliorates obesity and its complications by modulating gastric gene expression and inflammation. Methodology/Principal Findings: To test this hypothesis we examined the effects of gastric colonization on metabolic and inflammatory markers in mice infected with two isogenic strains of H. pylori: 26695 strain 98-325 (cagA+ wild-type) and its cag pathogenicity island (cagPAI) mutant strain 99-305, a knockout made by inserting a chloramphenicol resistance cassette. Only the cagPAI mutant decreased fasting blood glucose levels, improved glucose tolerance and suppressed weight gain in db/db mice and mice with diet-induced obesity. These effects were associated with increased gastric leptin levels, suppressed infiltration of macrophages, enhanced influx of regulatory T cells (Treg) in adipose tissue and suppressed gastric inflammation. Gene set enrichment analyses of gastric mucosal samples identified six differentially modulated pathways, including the Hedgehog signaling pathway that is associated with control of cellular proliferation and gastric carcinogenesis as well as the insulin signaling pathway. Conclusions/Significance: Gastric colonization with cagPAI-negative strains of H. pylori ameliorate obesity and inflammation by modulating gastric gene expression, suggesting that cag-negative H. pylori strains might be beneficial in ameliorating obesity and its co-morbidities. Gastric mucosa from three groups of mice: uninfected, infected with H. pylori 26695 strain 98-325 (cagA+ wild-type) or infected with H. pylori mutant strain 99-305 (lacking cag pathogenicity island; cagA-)
2010-11-13 | E-GEOD-21833 | biostudies-arrayexpress
Project description:H. pylori virulence factors have been suggested to be important in determining the outcome of infection. The H. pylori adhesion protein BabA2 is thought to play an crucial role in bacterial colonization and in induction of a severe gastric inflammation, particularly in combination with expression of CagA and VacA. However, the influence of these virulence factors on the pathogenesis of H. pylori infection, is still poorly understood. To address this question, the inflammatory gene expression profiles from two groups of patients infected with triple-negative strains (lacking expression of CagA, BabA2 and VacAs1, but expressing VacAs2) and triple-positive strains (expressing CagA, VacAs1 and BabA2, but lacking expression of VacAs2) were investigated. The gene expression pattern in the antrum gastric mucosa from patients infected with different H. pylori strains was very similar, and no differentially expressed genes could be identified by pair-wise comparisons. Our data thus suggest a lack of correlation between the host inflammatory responses in the gastric mucosa and expression of the BabA2, CagA and VacAs1 genes. Keywords: diseases analysis
2008-05-01 | GSE6143 | GEO