ArticleInfection and immunity2007
Helicobacter pylori VacA enhances prostaglandin E2 production through induction of cyclooxygenase 2 expression via a p38 mitogen-activated protein kinase/activating transcription factor 2 cascade in AZ-521 cells.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Vacuolating Cytotoxin A (VacA) and Extracellular Vesicles inIranian journal of pathology · 2025Review
- Developing a potent vaccine againstExpert reviews in molecular medicine · 2024Review
- Article
- Helicobacter pylori infection and Parkinson's Disease: etiology, pathogenesis and levodopa bioavailability.Immunity & ageing : I & A · 2024Review
- Chronic inflammation and long-lasting changes in the gastric mucosa after Helicobacter pylori infection involved in gastric cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
- Amoxicillin and Clarithromycin Mucoadhesive Delivery System forPharmaceutics · 2021Article
- Article
- Resveratrol mitigates lipopolysaccharide-mediated acute inflammation in rats by inhibiting the TLR4/NF-κBp65/MAPKs signaling cascade.Scientific reports · 2017Article
- Pleiotropic cytotoxicity of VacA toxin in host cells and its impact on immunotherapy.BioImpacts : BI · 2017Review
- Helicobacter pylori VacA, acting through receptor protein tyrosine phosphatase α, is crucial for CagA phosphorylation in human duodenum carcinoma cell line AZ-521.Disease models & mechanisms · 2016Article
- Review
- Intracellular colon cancer-associated Escherichia coli promote protumoral activities of human macrophages by inducing sustained COX-2 expression.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- Helicobacter pylori infection, gastrin and cyclooxygenase-2 in gastric carcinogenesis.World journal of gastroenterology · 2014Review
- Remodeling the host environment: modulation of the gastric epithelium by the Helicobacter pylori vacuolating toxin (VacA).Frontiers in cellular and infection microbiology · 2012Review
- Helicobacter pylori VacA reduces the cellular expression of STAT3 and pro-survival Bcl-2 family proteins, Bcl-2 and Bcl-XL, leading to apoptosis in gastric epithelial cells.Digestive diseases and sciences · 2011Article
- Relevance of Helicobacter pylori genotypes in gastric pathology and its association with plasma malondialdehyde and nitric oxide levels.Inflammopharmacology · 2010Article
- A Tale of Two Toxins: Helicobacter Pylori CagA and VacA Modulate Host Pathways that Impact Disease.Frontiers in microbiology · 2010Article
- Involvement of mitogen-activated protein kinases and nuclear factor kappa B pathways in signaling COX-2 expression in chronic rhinosinusitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2009Article
- Helicobacter pylori-induced interleukin-12 p40 expression.Infection and immunity · 2009Article
- Helicobacter pylori VacA-induced inhibition of GSK3 through the PI3K/Akt signaling pathway.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
12 authors at 8 institutions in 3 countries.
Funding
Abstract
Treatment of AZ-521 cells with Helicobacter pylori VacA increased cyclooxygenase 2 (COX-2) mRNA in a time- and dose-dependent manner. A p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580, blocked elevation of COX-2 mRNA levels, whereas PD98059, which blocks the Erk1/2 cascade, partially suppressed the increase. Consistent with involvement of p38 MAPK, VacA-induced accumulation of COX-2 mRNA was reduced in AZ-521 cells overexpressing a dominant-negative p38 MAPK (DN-p38). Phosphatidylinositol-specific phospholipase C, which inhibits VacA-induced p38 MAPK activation, blocked VacA-induced COX-2 expression. In parallel with COX-2 expression, VacA increased prostaglandin E(2) (PGE(2)) production, which was inhibited by SB203580 and NS-398, a COX-2 inhibitor. VacA-induced PGE(2) production was markedly attenuated in AZ-521 cells stably expressing DN-p38. VacA increased transcription of a COX-2 promoter reporter gene and activated a COX-2 promoter containing mutated NF-kappaB or NF-interleukin-6 sites but not a mutated cis-acting replication element (CRE) site, suggesting direct involvement of the activating transcription factor 2 (ATF-2)/CREB-binding region in VacA-induced COX-2 promoter activation. The reduction of ATF-2 expression in AZ-521 cells transformed with ATF-2-small interfering RNA duplexes resulted in suppression of COX-2 expression. Thus, VacA enhances PGE(2) production by AZ-521 cells through induction of COX-2 expression via the p38 MAPK/ATF-2 cascade, leading to activation of the CRE site in the COX-2 promoter.
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Registered trials
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