SynthesisWorld journal of gastroenterology2015
Interleukin-18 genetic polymorphisms contribute differentially to the susceptibility to Crohn's disease.
Synthesis in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Interleukin-18 Gene Polymorphisms and Rheumatoid Arthritis Susceptibility: An Umbrella Review of Meta-Analyses.Journal of immunology research · 2024Pooled it
- Urolithin A activates aryl hydrocarbon receptor-NLRP6-mediated pathways in intestinal epithelial cells to modulate mucosal immunity and strengthen gut barrier integrity.Nature communications · 2026Article
- Article
- Interleukin-18 binding protein deficiency results in gut microbiota dysbiosis and aggravated diet-induced MASH in mice.JHEP reports : innovation in hepatology · 2026Article
- Inflammasomes in Intestinal Disease: Mechanisms of Activation and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- LRRK2 G2019S Promotes Colon Cancer Potentially via LRRK2-GSDMD Axis-Mediated Gut Inflammation.Cells · 2024Article
- NOD-like Receptor Signaling Pathway in Gastrointestinal Inflammatory Diseases and Cancers.International journal of molecular sciences · 2023Review
- Association ofFrontiers in pediatrics · 2023Article
- IL-36γ and IL-36Ra Reciprocally Regulate Colon Inflammation and Tumorigenesis by Modulating the Cell-Matrix Adhesion Network and Wnt Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- IL-22 initiates an IL-18-dependent epithelial response circuit to enforce intestinal host defence.Nature communications · 2022Article
- Interleukin-18 in metabolism: From mice physiology to human diseases.Frontiers in endocrinology · 2022Review
- Dysregulated inflammasome activity in intestinal inflammation - Insights from patients with very early onset IBD.Frontiers in immunology · 2022Review
- Enteric Glial Cells in Immunological Disorders of the Gut.Frontiers in cellular neuroscience · 2022Review
- Inflammasomes and Colorectal Cancer.Cells · 2021Review
- The association of rs187238, rs19465518 and rs1946519 IL-8 polymorphisms with acute kidney injury in preterm infants.BioMedicine · 2021Article
- Contradictory Effects of NLRP3 Inflammasome Regulatory Mechanisms in Colitis.International journal of molecular sciences · 2020Review
- Interleukin-18 in Health and Disease.International journal of molecular sciences · 2019Review
- IL-33 and IL-18 in Inflammatory Bowel Disease Etiology and Microbial Interactions.Frontiers in immunology · 2019Review
- NLRP3 Inflammasome and Inflammatory Bowel Disease.Frontiers in immunology · 2019Review
- Inflammasome, Inflammation, and Tissue Homeostasis.Trends in molecular medicine · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the correlation between interleukin-18 (IL-18) gene polymorphisms and the risk of developing Crohn's disease (CD).
methodsThe PubMed, CISCOM, CINAHL, Web of Science, EBSCO, Cochrane Library, MEDLINE, EMBASE and CBM databases were searched without any language restrictions using combinations of keywords relating to CD and IL-18 for relevant articles published before November 1(st), 2013. Screening of the published studies retrieved from searches was based on our stringent inclusion and exclusion criteria and resulted in seven eligible studies for meta-analysis. A meta-analysis was conducted using a random-effects model with STATA 12.0 software. Crude odds ratios (ORs) with 95% confidence intervals (95%CI) were calculated.
resultsSeven case-control studies, with a total of 1930 CD cases and 1930 healthy subjects, met our inclusion criteria. The results of our meta-analysis indicated that the IL-18 rs1946518 A>C and rs187238 G>C polymorphisms may correlate with an increased risk of CD under five genetic models (all P < 0.05). Furthermore, we observed positive associations between the IL-18 rs360718 A>C polymorphism and CD risk under three genetic models (C allele vs A allele: OR = 2.03, 95%CI: 1.20-3.43, P = 0.008; CC vs AA+AC: OR = 2.39, 95%CI: 1.2-4.43, P = 0.006; CC vs AC: OR = 2.31, 95%CI: 1.22-4.38, P = 0.010). However, such associations were not found for the IL-18 rs917997 C>T, codon 35 A>C and rs1946519 G>T polymorphisms (all P > 0.05). A subgroup analysis was conducted to investigate the effect of ethnicity on an individual's susceptibility to CD. Our results revealed positive correlations between IL-18 genetic polymorphisms and an increased risk of CD among Asians and Africans (all P < 0.05), but not among Caucasians (all P > 0.05).
conclusionThis meta-analysis indicated that the IL-18 rs1946518 A>C, rs187238 G>C and rs360718 A>C polymorphisms may contribute to susceptibility to CD, especially among Asians and Africans. These polymorphisms are known to reduce IL-18 mRNA and protein levels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.