ArticleThe Journal of infectious diseases2008
Levels of interleukin-18 are markedly increased in Helicobacter pylori-infected gastric mucosa among patients with specific IL18 genotypes.
Article in The Journal of infectious diseases, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 27 citations in OpenAlex.
- Polymorphism in the Promoter Region of theFrontiers in immunology · 2020Trial
- A SpecificFrontiers in immunology · 2020Trial
- NOD1 mediates interleukin-18 processing in epithelial cells responding to Helicobacter pylori infection in mice.Nature communications · 2023Article
- The Role of Gastric Mucosal Immunity in Gastric Diseases.Journal of immunology research · 2020Review
- IL18 Gene Variants Influence the Susceptibility to Chagas Disease.PLoS neglected tropical diseases · 2016Article
- Association Between IL-17, IL-8 and IL-18 Expression in Peripheral Blood and Helicobacter Pylori Infection in Mongolian Gerbils.Jundishapur journal of microbiology · 2015Article
- Association between interleukin-18 gene polymorphism and Helicobacter pylori infection in the Korean population.Scientific reports · 2015Article
- IL-18 Gene Promoter Region 607C/A Polymorphism in HIV-1 Infected North Indian Population.Balkan journal of medical genetics : BJMG · 2011Article
- Gastric mucosal interleukin-17 and -18 mRNA expression in Helicobacter pylori-induced Mongolian gerbils.Cancer science · 2009Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThe cellular immune response in gastric mucosa infected with Helicobacter pylori is proposed to be predominantly of the T helper cell type 1 type.
methodsInterleukin (IL)-18, IL-12, and interferon (IFN)-gamma levels were measured in gastric mucosal biopsy specimens by reverse-transcription polymerase chain reaction (PCR) and by enzyme-linked immunosorbent assay; IL18 polymorphisms were determined by PCR.
resultsBiopsy specimens from 128 patients (56 with nonulcer dyspepsia, 28 with gastric ulcers, 28 with duodenal ulcers, and 16 with gastric cancer) were examined; 96 patients had H. pylori infection. IL-18 levels were markedly up-regulated in mucosa infected with H. pylori (P < .001), whereas IL-12 and IFN-gamma levels were independent of H. pylori status. IL-18 levels correlated with IFN-gamma levels only in infected patients (R = 0.31 to R = 0.51). IL-18 levels were the determining factor for monocyte infiltration in H. pylori-infected mucosa (P < .001). H. pylori-infected patients displaying IL18 -607C/C and -137G/G had higher IL-18 levels than did those with other genotypes and were more likely to experience treatment failure.
conclusionH. pylori infection induces IL-18 in the gastric mucosa. H. pylori-infected patients with IL18 -607C/C and -137G/G have higher IL-18 levels, which causes severe gastric inflammation. IL18 genotype might be a marker for predicting the effects of eradication therapy.
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