Transcriptome of Helicobacter pylori in presence or absence of the cagPAI
Ontology highlight
ABSTRACT:
ORGANISM(S): Helicobacter pylori
PROVIDER: GSE227450 | GEO | 2023/04/21
REPOSITORIES: GEO
Similar Datasets
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.
2017-02-10 | GSE67270 | GEO
Project description:Helicobacter pylori conquered the world by colonizing the human stomach. There are two major groups of strains, one with and one without a cag pathogenicity island (cagPAI), which result in different clinical outcomes with increased severity in cagPAI+ H. pylori infections such as higher inflammation and higher rates of gastric carcinogenesis. Since the gastro-intestinal tract is bombarded with nonspecific ligands that would induce innate signaling, tissue-resident immune cells are believed to lack toll-like receptor (TLR) signaling (anergy).To illuminate how anergic innate immune cells respond to H. pylori, we first investigated the transcriptome of H. pylori infected wild type and MyD88/Trif -/- macrophages, which lack TLR signaling. We observed that the majority of regulated genes in wt macrophages were dependent on TLR signaling. In addition, we found that some of the upregulated genes changed their kinetic behavior depending on TLR signaling. Only anergic macrophages were able to differentiate between cagPAI+ and cagPAI- H. pylori via their transcriptional kinetics of specific early response genes. These genes showed a strong bias towards adenylate-uridylate-rich elements (AREs) containing genes, including the prominent pro-inflammatory cytokines IL-1beta and TNF-alpha. Differentiation was dependent on the presence of the cag type 4 secretion system (cagT4SS), but not the CagA effector protein. Thus, we speculate that the direct recognition of the secretion system by tissue-resident macrophages enables the host to differentiate between pathogenic (cagPAI+) and commensal (cagPAI-) H. pylori variants.
2015-09-01 | GSE56791 | GEO
Project description:Differential gene transcript amounts between Helicobacter pylori N6 (wild type strain) bacteria and isogenic tlpD mutant grown in liquid culture to similar O.D.600 (1.0; mid log)
2016-04-15 | GSE79364 | GEO
Project description:In this study, we tested the hypothesis that high salt concentrations might alter gene expression in H. pylori. Analysis here provides into the role that salt may play in H. pylori pathogenesis. . H. pylori strain 26695 (SC#7) was grown for 15 h in BB-FBS medium containing 0.5% sodium chloride (i.e. BB-FBS-0.5%) The bacterial cells were then grown for 10 h, in fresh brucella broth at either 0.25% or 1.5% salt, harvested by centrifugation, and frozen at -80oC. RNA isolated was reverse transcribed and used to probe H. pylori Panorama arrays
2010-06-25 | E-GEOD-7183 | biostudies-arrayexpress
Project description:Background: Penicillins inhibit cell wall synthesis; therefore, H. pylori must be dividing for these antibiotics to be effective. Identifying growth responses to varying medium pH may allow design of more effective treatment regimens. Aim: To determine the effect of acidity on bacterial growth and the bactericidal efficacy of ampicillin. Methods: H. pylori were incubated in dialysis chambers suspended in 1.5L of media at various pHs with 5mM urea, with or without ampicillin, for 4, 8 or 16 hours, thus mimicking unbuffered gastric juice. Changes in gene expression, viability and survival were determined. The bacterial load of H. pylori infected gerbils was determined with and without profound acid inhibition. Results: At pH 3.0, but not at pH 4.5 or 7.4, there was decreased expression of ~400 genes, including many cell envelope biosynthesis, cell division genes and penicillin-binding proteins. In the presence of ampicillin, viability and survival declined at pH 4.5 and 7.4 but not at pH 3.0. Profound acid inhibition of H. pylori infected gerbils increased the antral bacterial load >3 fold, showing that elevation of intragastric pH stimulated growth. Conclusions: Ampicillin is bactericidal at pH 4.5 and 7.4, but not at pH 3.0, due to decreased expression of cell envelope and division genes at pH 3.0. Therefore, at pH 3.0, the pH at the gastric surface, the bacteria are non-dividing and persist with ampicillin treatment. A more effective inhibitor of acid secretion that maintains gastric pH near neutrality for 24 hours/day should enhance the efficacy of triple therapy and of amoxicillin, even allowing dual therapy for H. pylori eradication.
2012-09-30 | GSE39512 | GEO
Project description:Helicobacter pylori (H. pylori) is a highly successful pathogen that constitutes a serious threat to human health. However, the dynamic interaction between H. pylori and human gastric epithelium has not been fully documented. Here, by leveraging the advantage of dual RNA sequencing technology, we characterized a cytotoxin-associated genes A (CagA)-modulated bacterial adoption strategy by reinforcing the expression of ATP-binding cassette (ABC) transporter-related genes, metQ and HP_0888 upon co-culturing with human gastric epithelial cells (GES-1), thus, to benefit intracellular H. pylori survival through facilitating the uptake of host-provided nutrients. We further detected a generally repressed impact on electron transportation-associated genes by CagA, leading to the activation of oxidative phosphorylation. Temporal profiling of host mRNA signatures revealed down-regulation of multiple splicing regulators elicited by bacterial infection. Consequently, aberrant pre-mRNA splicing of functional genes that were involved in cell cycle process in response to H. pylori infection were identified. Moreover, we verified a protective effect for gastric H. pylori colonization against chronic dextran sulfate sodium (DSS)-induced colitis. Mechanistically, we profiled a cluster of short chain fatty acids (SCFA)-producing bacteria, Muribaculaceae that was selectively enriched in H. pylori-pre-colonized mice colon, contributing to the restoration of intestinal barrier function damaged by DSS treatment. Taken together, this study represents the first dual-transcriptome analysis of H. pylori during dynamic interaction with gastric epithelium and provide new insights into H. pylori pathogenesis.
2023-09-19 | GSE243405 | GEO
Project description:Helicobacter pylori is a common bacterial infection. It can lead to severe stomach problems, including stomach cancer. Researchers want to look at samples of the bacteria. These H. pylori strains will be taken from chronically infected people. They want to identify the genetic and epigenetic differences in H. pylori strains. This could help predict which people who get infected with the bacteria will get stomach cancer. This could lead to the cancer being detected earlier. It could also mean less people get stomach cancer.
Objectives:
To study genetic variations of H. pylori strains based on samples from chronically infected people. To identify the features of strains that might lead to severe stomach problems or stomach cancer.
Eligibility:
People ages 30-70 years who need an upper endoscopy or who were recently diagnosed with stomach cancer
Design:
Participants will be screened by the doctor who does their procedure and a study nurse.
Participants who have endoscopy will have ~6 biopsies removed. These are tissue samples. They are about the size of a grain of rice. Participants will allow the study team to access reports from their stomach exam.
Participants with stomach cancer will donate some of the tissue that will be removed during their clinical care. They will allow the study team to access reports of their surgery. They will also allow them to access the microscope slides of their stomach.
| 2216372 | ecrin-mdr-crc
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.
2010-05-26 | E-GEOD-10261 | biostudies-arrayexpress
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.
2012-04-30 | GSE30042 | GEO
Project description:Helicobacter pylori, a bacterium that colonizes the human stomach, like all Gram-negative bacteria spontaneously shed outer membrane vesicles (OMVs). OMVs, which act as a delivery system for bacterial components, are involved in bacterial-host interactions and thus contribute to pathogenesis. In this study, to understand the gene expression changes that human gastric epithelial cells might undergo when exposed to H. pylori-OMVs, we profiled the transcriptomic changes of the MKN74 gastric cell line induced by OMVs compared to control cells and H. pylori-infected cells, using the Ion AmpliSeq™ Transcriptome Human Gene Expression Panel. The top enriched pathways in the OMVs challenge condition included amino acid-related metabolic pathways, mitogen-activated protein kinase signaling, autophagy, and ferroptosis. The cell cycle, DNA replication, and repair pathways were the top diminished pathways. The transcriptomic changes induced by OMVs were largely consistent with those of the bacteria, although often at low expression levels, suggesting that their effects will mostly reinforce those of the bacterium itself. Our data provide a valuable portrayal of the transcriptomic remodeling of gastric cells by H. pylori-OMVs, which can be further dissected regarding the underlying molecular mediators and explored to understand the pathobiology of the full-spectrum of H. pylori-mediated diseases.
2024-04-03 | GSE229512 | GEO