ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Regulation of IL-18 in Helicobacter pylori infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 64 citations in OpenAlex.
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- Autophagy-Related GeneJournal of clinical medicine · 2024Article
- NOD-like Receptor Signaling Pathway in Gastrointestinal Inflammatory Diseases and Cancers.International journal of molecular sciences · 2023Review
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- Knockdown of ELF4 aggravates renal injury in ischemia/reperfusion mice through promotion of pyroptosis, inflammation, oxidative stress, and endoplasmic reticulum stress.BMC molecular and cell biology · 2023Article
- NOD1 mediates interleukin-18 processing in epithelial cells responding to Helicobacter pylori infection in mice.Nature communications · 2023Article
- Polymorphism in autophagy-related genes LRP1 and CAPZA1 may promote gastric mucosal atrophy.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Article
- Epithelial Pyroptosis in Host Defense.Journal of molecular biology · 2022Review
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- Downregulation of IRF2 Alleviates Sepsis-Related Acute Kidney Injury in vitro and in vivo.Drug design, development and therapy · 2021Article
- The Overexpression of Sirtuin1 (SIRT1) Alleviated Lipopolysaccharide (LPS)-Induced Acute Kidney Injury (AKI) via Inhibiting the Activation of Nucleotide-Binding Oligomerization Domain-Like Receptors (NLR) Family Pyrin Domain Containing 3 (NLRP3) Inflammasome.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Association between interleukin-18 gene polymorphism and Helicobacter pylori infection in the Korean population.Scientific reports · 2015Article
- Heme oxygenase-1 dysregulates macrophage polarization and the immune response to Helicobacter pylori.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Cytokines, cytokine gene polymorphisms and Helicobacter pylori infection: friend or foe?World journal of gastroenterology · 2014Review
- Enhanced expression of activation-induced cytidine deaminase in human gastric mucosa infected by Helicobacter pylori and its decrease following eradication.Journal of gastroenterology · 2014Article
- TLR2 and Nod2 mediate resistance or susceptibility to fatal intracellular Ehrlichia infection in murine models of ehrlichiosis.PloS one · 2013Article
- Article
- The local immune response of mice after Helicobacter suis infection: strain differences and distinction with Helicobacter pylori.Veterinary research · 2012Article
- Arginine and polyamines in Helicobacter pylori-induced immune dysregulation and gastric carcinogenesis.Amino acids · 2012Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
The gastric mucosal immune response is thought to be comprised predominantly of the Th1 type; however, there are limited data regarding the role of IL-18 in Helicobacter pylori-induced inflammation. We investigated IL-18 levels in gastric mucosal biopsy specimens as well as in isolated gastric epithelial cells and lamina propria mononuclear cells. We also investigated IL-18 levels in gastric epithelial cells and the monocyte cell line THP-1 cocultured with H. pylori. In both systems, IL-18 levels were markedly enhanced in H. pylori-infected epithelial cells and monocytes. IL-18 levels in H. pylori-infected gastric mucosa were well correlated with the severity of gastric inflammation, confirming that H. pylori-induced IL-18 plays an important role in gastric injury. Virulence factors of H. pylori; the cag pathogenicity island and OipA affected IL-18 induction in different manners. Up-regulation of IL-18 mRNA/protein in epithelial cells was dependent on both virulence factors. Interestingly, up-regulation of IL-18 mRNA in monocytes was independent of both factors, whereas IL-18 protein was OipA dependent-cag pathogenicity island independent, indicating that OipA regulates IL-18 induction in monocytes at the posttranscriptional level. IL-18 levels in the gastric biopsy specimens showed similar patterns to those in lamina propria mononuclear cells with respect to virulence factors, suggesting that submucosal monocytes/macrophages are the main source of IL-18 induced by H. pylori infection. H. pylori appeared to regulate the ERK/JNK-->AP-1 pathway in both cell types. In addition, OipA and its related p38 pathway may be closely involved in IL-18 induction in H. pylori-infected gastric mucosa and may contribute to gastric injury.
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