ArticleCellular microbiology2007
Helicobacter pylori environmental interactions: effect of acidic conditions on H. pylori-induced gastric mucosal interleukin-8 production.
Article in Cellular microbiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Comparative genomics of two Vietnamese Helicobacter pylori strains, CHC155 from a non-cardia gastric cancer patient and VN1291 from a duodenal ulcer patient.Scientific reports · 2023Article
- Article
- Integrin engagement by the helical RGD motif of the Helicobacter pylori CagL protein is regulated by pH-induced displacement of a neighboring helix.The Journal of biological chemistry · 2015Article
- Outer membrane inflammatory protein A, a new virulence factor involved in the pathogenesis of Helicobacter pylori.Molecular biology reports · 2014Article
- Helicobacter pylori virulence and cancer pathogenesis.Future oncology (London, England) · 2014Review
- Helicobacter pylori impedes acid-induced tightening of gastric epithelial junctions.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Helicobacter pylori-associated regulation of forkhead transcription factors FoxO1/3a in human gastric cells.Helicobacter · 2012Article
- Vibrio parahaemolyticus infection induces modulation of IL-8 secretion through dual pathway via VP1680 in Caco-2 cells.The Journal of infectious diseases · 2011Article
- Mechanisms of disease: Helicobacter pylori virulence factors.Nature reviews. Gastroenterology & hepatology · 2010Review
- Helicobacter pylori activate epidermal growth factor receptor- and phosphatidylinositol 3-OH kinase-dependent Akt and glycogen synthase kinase 3beta phosphorylation.Cellular microbiology · 2009Article
- OipA plays a role in Helicobacter pylori-induced focal adhesion kinase activation and cytoskeletal re-organization.Cellular microbiology · 2008Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
To explore the interactions between the host, environment and bacterium responsible for the different manifestations of Helicobacter pylori infection, we examined the effect of acidic conditions on H. pylori-induced interleukin (IL)-8 expression. AGS gastric epithelial cells were exposed to acidic pH and infected with H. pylori[wild-type strain, its isogenic cag pathogenicity island (PAI) mutant or its oipA mutant]. Exposure of AGS cells to acidic pH alone did not enhance IL-8 production. However, following exposure to acidic conditions, H. pylori infection resulted in marked enhancement of IL-8 production which was independent of the presence of the cag PAI and OipA, indicating that H. pylori and acidic conditions act synergistically to induce gastric mucosal IL-8 production. In neutral pH environments H. pylori-induced IL-8 induction involved the NF-kappaB pathways, the extracellular signal-regulated kinase (ERK)-->c-Fos/c-Jun-->activating protein (AP-1) pathways, JNK-->c-Jun-->AP-1 pathways and the p38 pathways. At acidic pH H. pylori-induced augmentation of IL-8 production involved markedly upregulated the NF-kappaB pathways and the ERK-->c-Fos-->AP-1 pathways. In contrast, activation of the JNK-->c-Jun-->AP-1 pathways and p38 pathways were pH independent. These results might explain the clinical studies in which patients with duodenal ulcers had higher levels of IL-8 in the antral gastric mucosa than patients with simple H. pylori gastritis.
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