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- Title
Helicobacter pylori environmental interactions: effect of acidic conditions on H. pylori-induced gastric mucosal interleukin-8 production.
- Authors
Il Ju Choi; Fujimoto, Saori; Yamauchi, Kazuyoshi; Graham, David Y.; Yamaoka, Yoshio
- 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-κB 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-κB 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.
- Subjects
HELICOBACTER pylori; GASTRIC mucosa; PHYSIOLOGICAL effects of acids; EPITHELIAL cells; INTERLEUKIN-8; HYDROGEN-ion concentration; EXTRACELLULAR enzymes; DUODENAL ulcers; CELL physiology
- Publication
Cellular Microbiology, 2007, Vol 9, Issue 10, p2457
- ISSN
1462-5814
- Publication type
Article
- DOI
10.1111/j.1462-5822.2007.00973.x