The role of TRAF1 in Helicobacter pylori infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE290844 | GEO | 2025/03/05
REPOSITORIES: GEO
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Project description:Our previous studies have shown thatHelicobacter pylori can induce the expression of OASL, which plays a crucial role in gastritis-cancer progression. In order to further investigate the detailed mechanism of OASL, we constructed an OASL overexpression model in HGC27 cells.
2025-03-19 | GSE291766 | 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 is an important human pathogen that infects the human gastric mucosa leading to chronic inflammation which is responsible for severe gastroduodenal diseases. The Outer Inflammatory Protein A (OipA) of H. pylori is an important virulence factor. However, the role of OipA in gastric cancer and ulcer development is still not well-established. Phase variation within a CT dinucleotide repeat motif of oipA switches its expression “on” and “off”. This study aims to elucidate the role of OipA in H. pylori infection using oipA “on” and “off” clinical strains and oipA deletion mutant. Methods: Proteomics analysis was performed on AGS human gastric epithelial cell line post-infection with oipA “on” and “off” H. pylori using liquid chromatography / mass spectrometry (LC/MS). In addition, AGS apoptosis and cell cycle assays were performed. To confirm the findings, oipA deletion mutant (ΔoipA) was generated and expression of VacA was detected using Western blotting. Result: Expression of AGS proteins involve in human disease was suppressed / down-regulated post-infection with oipA “off” strains, as well as oipA mutant, compared to oipA “on” strains. Furthermore, oipA “off” strains and oipA mutant resulted in a higher level of apoptosis and G0/G1 cell-cycle arrest in AGS cells than oipA “on” strains. Interestingly, deletion of oipA was found to increase VacA production by the bacterium. Discussion: The capability of oipA “off” strains to induce apoptosis and suppress proteins having roles in human disease may suggest that these H. pylori may be less virulent or may even be protective against carcinogenesis compared to its oipA “on” counterparts. This may potentially explain the higher incidence of gastric cancer among East Asian which oipA “on” strains predominates. Conclusions: Data from this study strengthened our understanding of the role of H. pylori OipA as a virulence factor in chronic inflammation, metastasis and carcinogenesis.
2022-03-14 | PXD005020 | Pride
Project description:Background Gastric Helicobacter pylori colonization leads to iron deficiency anemia (IDA), especially in children and adolescents. However the pathogenesis is poorly understood. Objective We sought to identify specific H. pylori genes involved in IDA development, by comparing bacterial genome-wide expression profiling in patients affected or not. Methods H. pylori were isolated from four children with IDA and four from matched controls without IDA. Based on these isolates, cDNA microarrays under iron-replete or depleted conditions were systematically performed to compare gene expression profiles at the whole genome level. Real-time reverse-transcription (RT-) PCR and protein assays were performed for further assessing the profile differentiation of the identified H. pylori IDA-associated genes. Results We identified 29 and 11 genes with significantly higher or lower expression in the IDA isolates compared to non-IDA isolates, respectively. Especially notable were higher expression of sabA gene encoding sialic acid-binding adhesin in the IDA isolates, which was confirmed by real-time RT-PCR study. Moreover, iron-depletion in vitro led to up-regulation of fecA1 and frpB1 genes and down-regulation of pfr, as predicted. Known iron-regulated genes such as fur, pfr, fecA, and feoB did not significantly differ between both groups. The IDA isolates had significantly higher expression of vacuolating cytotoxin gene vacA than non-IDA isolates, consistent with the results of VacA protein assays. There were no significant differences in bacterial growth value between IDA and non-IDA isolates. Conclusions It is likely that H. pylori carrying high expression of sabA causes IDA, especially in children and adolescents who have increased daily iron demand. In addition, it is possible that several host-interactive genes, including vacA, may play a synergistic role for sabA in IDA development.
2017-07-25 | GSE101807 | 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.
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
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.
2020-05-26 | PXD010082 | Pride
Project description:Transcriptome analysis of AGS cells infected with Helicobacter pylori P12
2018-09-17 | GSE73226 | GEO
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: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.
2012-12-28 | GSE39490 | GEO