Helicobacter pylori environmental interactions: effect of acidic conditions on H. pylori-induced gastric mucosal interleukin-8 production

• Published in: Cellular microbiology Vol. 9; no. 10; pp. 2457 - 2469
• Main Authors: Choi, Il Ju, Fujimoto, Saori, Yamauchi, Kazuyoshi, Graham, David Y, Yamaoka, Yoshio
• Format: Journal Article
• Language: English
• Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.10.2007; Blackwell Publishing Ltd; Hindawi Limited
• Subjects: Cell Line; Duodenal Ulcer - metabolism; Duodenal Ulcer - microbiology; Epithelial Cells - metabolism; Epithelial Cells - microbiology; Gastric Mucosa - metabolism; Gastric Mucosa - microbiology; Gastritis - metabolism; Gastritis - microbiology; Helicobacter Infections - microbiology; Helicobacter pylori - physiology; Humans; Hydrogen-Ion Concentration; Interleukin-8 - biosynthesis; Signal Transduction
• ISSN: 1462-5814; 1462-5822
• DOI: 10.1111/j.1462-5822.2007.00973.x

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)[rightward arrow]c-Fos/c-Jun[rightward arrow]activating protein (AP-1) pathways, JNK[rightward arrow]c-Jun[rightward arrow]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[rightward arrow]c-Fos[rightward arrow]AP-1 pathways. In contrast, activation of the JNK[rightward arrow]c-Jun[rightward arrow]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.