ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2013
Induction of COX-2 expression by Helicobacter pylori is mediated by activation of epidermal growth factor receptor in gastric epithelial cells.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Treatment with (R)-α-methylhistamine or IL4 stimulates mucin production and decreasesVirulence · 2025Article
- Fuzi polysaccharides improve immunity in immunosuppressed mouse models by regulating gut microbiota composition.Heliyon · 2023Article
- Roles of Eicosanoids in Regulating Inflammation and Neutrophil Migration as an Innate Host Response to Bacterial Infections.Infection and immunity · 2021Article
- Nod1 Imprints Inflammatory and Carcinogenic Responses toward the Gastric PathogenCancer research · 2019Article
- Circulating Myeloid Derived Suppressor Cells (MDSC) That Accumulate in Premalignancy Share Phenotypic and Functional Characteristics With MDSC in Cancer.Frontiers in immunology · 2019Article
- Article
- Article
- Status of Epstein-Barr Virus Coinfection withJournal of oncology · 2017Review
- Pathogenic Helicobacter pylori strains translocate DNA and activate TLR9 via the cancer-associated cag type IV secretion system.Oncogene · 2016Article
- Structural Change in Microbiota by a Probiotic Cocktail Enhances the Gut Barrier and Reduces Cancer via TLR2 Signaling in a Rat Model of Colon Cancer.Digestive diseases and sciences · 2016Article
- Article
- Transforming growth factor-β: an important mediator in Helicobacter pylori-associated pathogenesis.Frontiers in cellular and infection microbiology · 2015Review
- The host protein calprotectin modulates the Helicobacter pylori cag type IV secretion system via zinc sequestration.PLoS pathogens · 2014Article
- Activation of EGFR and ERBB2 by Helicobacter pylori results in survival of gastric epithelial cells with DNA damage.Gastroenterology · 2014Article
- Helicobacter pylori infection: host immune response, implications on gene expression and microRNAs.World journal of gastroenterology · 2014Review
- Effects of EGFR Inhibitor on Helicobacter pylori Induced Gastric Epithelial Pathology in Vivo.Pathogens (Basel, Switzerland) · 2013Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic infection of the gastric mucosa by Helicobacter pylori is associated with an increased risk of developing gastric cancer; however, the vast majority of infected individuals never develop this disease. One H. pylori virulence factor that increases gastric cancer risk is the cag pathogenicity island, which encodes a bacterial type IV secretion system. Cyclooxygenase-2 (COX-2) expression is induced by proinflammatory stimuli, leading to increased prostaglandin E₂ (PGE₂) secretion by gastric epithelial cells. COX-2 expression is increased in gastric tissue from H. pylori-infected persons. H. pylori also activates the epidermal growth factor receptor (EGFR) in gastric epithelial cells. We now demonstrate that H. pylori-induced activation of COX-2 in gastric cells is dependent upon EGFR activation, and that a functional cag type IV secretion system and direct bacterial contact are necessary for full induction of COX-2 by gastric epithelial cells. PGE₂ secretion is increased in cells infected with H. pylori, and this induction is dependent on a functional EGFR. Increased apoptosis in response to H. pylori occurs in cells treated with a COX-2 inhibitor, as well as COX-2-/- cells, indicating that COX-2 expression promotes cell survival. In vivo, COX-2 induction by H. pylori is significantly reduced in mice deficient for EGFR activation compared with wild-type mice with a fully functional receptor. Collectively, these findings indicate that aberrant activation of the EGFR-COX-2 axis may lower the threshold for carcinogenesis associated with chronic H. pylori infection.
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