Ornithine Decarboxylase Activity in Gastric Epithelial Cells Contributes to the Pathogenesis of Helicobacter pylori
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE181917 | GEO | 2022/06/07
REPOSITORIES: GEO
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Project description:Colonization by H. pylori is associated with a wide range of gastric diseases, ranging from superficial gastritis to more severe pathologies, including intestinal metaplasia and adenocarcinoma. The interplay of the host response and the pathogen affect the outcome of disease. One major component of the mucosal response to H. pylori is the activation of a strong, but inefficient immune response that fails to control the infection and frequently causes tissue damage. We have shown that polyamines can regulate H. pylori-induced inflammation. Chemical inhibition of ornithine decarboxylase (ODC), which generates putrescine from L-ornithine, reduces gastritis in mice and adenocarcinoma incidence in gerbils infected with H. pylori. However, we have also demonstrated that Odc deletion in myeloid cells enhances M1 macrophage activation and gastritis. Here we used a genetic approach to assess the specific role of gastric epithelial ODC during H. pylori infection. Deletion of Odc in gastric epithelial cells reduces gastritis, attenuates epithelial proliferaton, alters the metabolome, and dowregulates the expression of immune mediators induced by H. pylori. Inhibition of ODC activity in gastric epithelial cells reduces H. pylori-induced NF-B activation and CXCL8 mRNA expression. Chronic inflammation is a major risk factor for the progression to more severe pathologies associated with H. pylori infection and we now show that epithelial ODC plays an important role in mediating this inflammatory response.
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Project description:Ornithine Decarboxylase Activity in Gastric Epithelial Cells Contributes to the Pathogenesis of Helicobacter pylori
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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.
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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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