Helicobacter pylori environmental interactions: effect of acidic conditions on H.pylori-induced gastric mucosal interleukin-8 production
SummaryTo 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 ac...
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Published in | Cellular microbiology Vol. 9; no. 10; pp. 2457 - 2469 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
01.10.2007
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Subjects | |
Online Access | Get full text |
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Summary: | SummaryTo 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-B pathways, the extracellular signal-regulated kinase (ERK)1c-Fos/c-Jun1activating protein (AP-1) pathways, JNK1c-Jun1AP-1 pathways and the p38 pathways. At acidic pH H.pylori-induced augmentation of IL-8 production involved markedly upregulated the NF-B pathways and the ERK1c-Fos1AP-1 pathways. In contrast, activation of the JNK1c-Jun1AP-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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 content type line 23 ObjectType-Feature-2 |
ISSN: | 1462-5814 1462-5822 |
DOI: | 10.1111/j.1462-5822.2007.00973.x |