Open AccessHelicobacter pylori environmental interactions: effect of acidic conditions on H. pylori‐ induced gastric mucosal interleukin‐8 production
Author(s) -
Choi Il Ju,
Fujimoto Saori,
Yamauchi Kazuyoshi,
Graham David Y.,
Yamaoka Yoshio
Publication year - 2007
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2007.00973.x
Subject(s) - helicobacter pylori , biology , extracellular , mutant , gastric mucosa , mapk/erk pathway , downregulation and upregulation , p38 mitogen activated protein kinases , microbiology and biotechnology , interleukin 8 , gastritis , helicobacter , signal transduction , stomach , biochemistry , immunology , cytokine , gene , genetics
Summary 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.