ArticleClinical and diagnostic laboratory immunology2002
Host cell responses to genotypically similar Helicobacter pylori isolates from United States and Japan.
Article in Clinical and diagnostic laboratory immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
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- A specific A/T polymorphism in Western tyrosine phosphorylation B-motifs regulates Helicobacter pylori CagA epithelial cell interactions.PLoS pathogens · 2015Article
- Outer membrane inflammatory protein A, a new virulence factor involved in the pathogenesis of Helicobacter pylori.Molecular biology reports · 2014Article
- Clarithromycin modulates Helicobacter pylori-induced activation of nuclear factor-κB through classical and alternative pathways in gastric epithelial cells.Clinical and experimental medicine · 2014Article
- Helicobacter pylori and interleukin-8 in gastric cancer.World journal of gastroenterology · 2013Review
- Helicobacter pylori: gastric cancer and beyond.Nature reviews. Cancer · 2010Review
- The cag PAI is intact and functional but HP0521 varies significantly in Helicobacter pylori isolates from Malaysia and Singapore.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2010Article
- Immune reactions against elongation factor 2 kinase: specific pathogenesis of gastric ulcer from Helicobacter pylori infection.Clinical & developmental immunology · 2009Article
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- Pathogenesis of Helicobacter pylori infection.Clinical microbiology reviews · 2006Review
- Causal role of Helicobacter pylori infection in gastric cancer.World journal of gastroenterology · 2006Review
- Regulation of interleukin-6 promoter activation in gastric epithelial cells infected with Helicobacter pylori.Molecular biology of the cell · 2005Article
- Gastric transcription profile of Helicobacter pylori infection in the rhesus macaque.Infection and immunity · 2004Article
- Functional analysis of the cag pathogenicity island in Helicobacter pylori isolates from patients with gastritis, peptic ulcer, and gastric cancer.Infection and immunity · 2004Article
- Helicobacter pylori outer membrane vesicles modulate proliferation and interleukin-8 production by gastric epithelial cells.Infection and immunity · 2003Article
- Polymorphisms of Helicobacter pylori HP0638 reflect geographic origin and correlate with cagA status.Journal of clinical microbiology · 2002Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Associations of Helicobacter pylori genotypes with disease differ between Western countries and Asia. Therefore, we directly compared histopathological and in vitro responses to clinical isolates with similar genotypes. Sixty-three cagA(+) vacAs1/m1 H. pylori isolates (United States, n = 24; Japan, n = 39) and eight cagA-negative vacAs2/m2 strains were incubated with AGS cells, and supernatants were assayed for interleukin-8 (IL-8) and for DNA fragmentation. CagA tyrosine phosphorylation in AGS cells and the sequence of the putative HP0638 (oipA) signal sequence region were determined for 22 representative strains. HP0638 and/or cag island mutant strains were created and examined in IL-8 and CagA tyrosine phosphorylation assays. Levels of IL-8 induction and DNA fragmentation were similar in the U.S. and Japanese cagA(+) vacAs1/m1 isolates. All 10 of the isolates with the highest IL-8 induction and 8 of the 10 isolates with the lowest IL-8 induction had an in-frame oipA open reading frame, and all 10 of the isolates with the highest IL-8 induction and 7 of the 10 isolates with the lowest IL-8 induction induced CagA tyrosine phosphorylation in AGS cells. Eight isolates from gastric ulcer patients induced significantly more apoptosis in vitro, and more severe gastritis and atrophy in vivo, than other Japanese isolates. Disruption of HP0638 did not affect IL-8 induction or CagA tyrosine phosphorylation. Thus, H. pylori cagA(+) vacAs1/m1 isolates from the United States and Japan induce similar IL-8 and apoptosis levels. Inactivation of HP0638 does not alter epithelial responses mediated by the cag island in vitro. Assessment of apoptosis in vitro identified a group of H. pylori isolates that induce more severe gastric inflammation and atrophy.
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