PTyr-CoIP HP/AGS - Quantitative analysis of H. pylori induced phosphotyrosine signaling upon infection.
Ontology highlight
ABSTRACT:
INSTRUMENT(S): LTQ Orbitrap
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Permanent Cell Line Cell, Cell Culture
SUBMITTER: 
Christian Koehler
LAB HEAD: Bernd Thiede
PROVIDER: PXD000722 | Pride | 2014-07-09
REPOSITORIES: Pride
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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.
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Project description:Enteric pathogens with low infectious doses rely on the ability to orchestrate expression of virulence and metabolism-associated genes in response to environmental cues for successful infection. Accordingly, the human pathogen enterohemorrhagic Escherichia coli (EHEC) employs a complex multifaceted regulatory network to link expression of type III secretion system (T3SS) factors to nutrient availability. While phosphorylation of histidine and aspartate on two-component system response regulators is recognized as an integral part of signaling, the involvement of phosphotyrosine-mediated control is minimally explored in Gram-negative pathogens. Our recent phosphotyrosine profiling study of E. coli revealed 342 proteins, indicating that phosphotyrosine modifications in bacteria are more prevalent than previously anticipated. Here, we demonstrate that tyrosine phosphorylation of a metabolite-responsive LacI/GalR family regulator, Cra, negatively affects T3SS expression in glycolytic conditions typical for the colon lumen environment where production of the T3SS is unnecessary. Our data suggest that Cra phosphorylation affects T3SS expression by modulating expression of ler, encoding the major activator of EHEC virulence gene expression. Phosphorylation of the Cra Y47 residue diminishes DNA-binding, thereby altering expression of metabolism and virulence-associated genes including those of the LEE pathogenicity island encoding the T3SS. Hence, phosphotyrosine-mediated regulation provides a mechanism to regulate Cra activity. Our data further suggest that tyrosine phosphorylation influences DNA binding by PurR and LacI, thereby phosphotyrosine-mediated control could provide a means to regulate DNA-binding of LacI/GalR family regulators in general. Our study provides an initial effort to unravel the role of phosphotyrosine-mediated global signaling in controlling the EHEC virulence potential
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Project description:H. pylori Outer membrane phospholipase A (OMPLA) has been suggested to play a role in the virulence of this bacterium. The aim of this study was to profile the most significant cellular pathways and biological processes affected in gastric epithelial cells during 24 hours of H. pylori exposure, and to study the inflammatory response to OMPLA+ and OMPLA- H. pylori variants
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Project description:Transcriptome analysis of AGS cells infected with Helicobacter pylori P12
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Project description:This study set out to identify global changes in gene expression in AGS gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point.
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Project description:This study set out to identify global changes in gene expression in AGS gastric epithelial cells following 8 hours stimulation with 10 μg/ml lipopolysaccharide (LPS) from the gastric pathogen H. pylori. Microarray analysis was used to compare changes in gene expression between cells treated with 10 μg/ml H. pylori LPS and untreated cells at the same time point. Total RNA was harvested from AGS cells following treatment with LPS for 8h or untreated cells at the same time-point. 2 independent experiments were carried out. RNA was labelled and hybridized to GeneChips to analyse changes in gene expression.
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Project description:We performed genome-wide mRNA and miRNA expression analysis in gastric epithelial cell line AGS infected with Helicobacter pylori at 100 Multiplicity of Infection (MOI), comparing the expression profile of infected cells with uninfected cells. Differentially expressed mRNAs and miRNAs were identified, which showed a 1.5 fold change in expression in infected cells compared to uninfected cells. We performed in silico analysis of miRNA-mRNA target interactions among the inversely correlated differentially expressed miRNAs and mRNAs, and performed functional enrichment analysis of the target genes, to identify important cellular pathways that reflect the patho-biology of H. pylori infected cells. Among the important miRNA-mRNA target pairs, PHLPP1, reported to be associated with poor prognosis in cancer, was predicted to be a putative target of miR-29b-1-5p. Therefore, we focused on the miR-29b-1-5p/PHLPP1 miRNA/target pair for detailed investigation into their role in H. pylori-mediated signalling in gastric epithelial cells. This study demonstrates that an integrated analysis of global mRNA and miRNA expression patterns, combined with miRNA-mRNA target prediction and functional analysis of miRNA target genes can yield an understanding of the critical pathways regulating the behaviour of gastric epithelial cells challenged with H. pylori.
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Project description:We performed genome-wide mRNA and miRNA expression analysis in gastric epithelial cell line AGS infected with Helicobacter pylori at 100 Multiplicity of Infection (MOI), comparing the expression profile of infected cells with uninfected cells. Differentially expressed mRNAs and miRNAs wered identified, which showed a 1.5 fold change in expression in infected cells compared to uninfected cells. We performed in silico analysis of miRNA-mRNA target interactions among the inversely correlated differentially expressed miRNAs and mRNAs, and performed functional enrichment analysis of the target genes, to identify important cellular pathways that reflect the patho-biology of H. pylori infected cells. Among the important miRNA-mRNA target pairs, PHLPP1, reported to be associated with poor prognosis in cancer, was predicted to be a putative target of miR-29b-1-5p. Therefore, we focused on the miR-29b-1-5p/PHLPP1 miRNA/target pair for detailed investigation into their role in H. pylori-mediated signalling in gastric epithelial cells. This study demonstrates that an integrated analysis of global mRNA and miRNA expression patterns, combined with miRNA-mRNA target prediction and functional analysis of miRNA target genes can yield an understanding of the critical pathways regulating the behaviour of gastric epithelial cells challenged with H. pylori.
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Project description:Helicobacter pylori infection promotes chronic inflammation and plethora of DNA damages including strand breaks, base alterations, point mutations, microsatellite instability and epigenetic alterations. The gastric epitheliaI cells, in order to prevent genomic instability, require an integrous DNA damage repair (DDR) machinery which, however, has been reported to be modulated by the infection. CagA is a major Hp virulence factor that deregulates host cell functions such as proliferation, apoptosis and chromosomal integrity. Its pathogenic activity is partly regulated by tyrosine phosphorylation on repeated EPIYA-motifs. Our aim was to identify putative effects of H. pylori infection and CagA protein on DDR machinery, investigating the transcriptome of AGS cells, infected with P12 H. pylori wild-type strain, as well as, its corresponding CagA knock-out and the CagA phosphorylation-defective mutant following tyrosine (EPIYA) substitution by phenylalanine (EPIFA) in the EPIYA-C motifs. Upon RNA-Sequencing on polyA-selected transcripts we performed Differential Expression Analysis, Pathway Enrichment Analysis and visualization on KEGG Pathway Maps per DDR mechanism. Key DDR components that were observed to be downregulated in a CagA-related manner were validated via Western Blot utilizing AGS and the non-cancerous GES1 cell lines. Transcriptome analysis revealed that a notable number of DDR genes were downregulated during H. pylori infection resulting to potential modulation of Base Excision Repair, Mismatch Repair and a more intricate deregulation of Nucleotide Excision Repair, Homologous Recombination and Non-Homologous End-Joining. CagA contributes to MUTYH, FEN1, APE1, POLD1 and LIG1 downregulation and those observations were verified on the protein expression level, with the exception of APE1 that was on contrary observed to be upregulated. Our study accentuates the role of CagA, as a significant contributor of the H. pylori infection-mediated DDR modulation, disrupting the balance between DNA damage introduction and repair thus favoring genomic instability and potentially contributing to gastric carcinogenesis.
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Project description:Helicobacter pylori enhances the risk for ulcer disease and gastric cancer, yet only a minority of H. pylori-colonized individuals develop disease. We examined the ability of two H. pylori isolates to induce differential host responses in vivo or in vitro, and then used an H. pylori whole genome microarray to identify bacterial determinants related to pathogenesis. Gastric ulcer strain B128 induced more severe gastritis, proliferation, and apoptosis in gerbil mucosa than did duodenal ulcer strain G1.1, and gastric ulceration and atrophy occurred only in B128+ gerbils. In vitro, gerbil-passaged B128 derivatives significantly increased IL-8 secretion and apoptosis compared with G1.1 strains. DNA hybridization to the microarray identified several strain-specific differences in gene composition including a large deletion of the cag pathogenicity island in strain G1.1. Partial and complete disruption of the cag island in strain B128 attenuated induction of IL-8 in vitro and significantly decreased gastric inflammation in vivo. These results indicate that the ability of H. pylori to regulate epithelial cell responses related to inflammation depends on the presence of an intact cag pathogenicity island. Use of an H pylori whole genome microarray is an effective method to identify differences in gene content between H. pylori strains that induce distinct pathological outcomes in a rodent model of H. pylori infection. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
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