Journal Article10.1111/J.1399-0039.2005.00336.X
Association of interleukin-18 gene single-nucleotide polymorphisms with susceptibility to inflammatory bowel disease.
Yoshio Aizawa,Satoshi Sutoh,Mika Matsuoka,Michiko Negishi,Akira Torii,Yoshinari Miyakawa,H. Sugisaka,M. Nakamura,Toda G +8 more
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TL;DR: It was concluded that SNPs at the 5'-end of IL-18 gene might be closely related to the etiology of IBD.
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Abstract: Interleukin-18 (IL-18) is believed to be one of the most important cytokines in the pathogenesis of inflammatory bowel disease (IBD). The aim of the study was to clarify the significance of single-nucleotide polymorphisms (SNPs) at the 5′-end of the IL-18 gene in the development of IBD. DNA was obtained from peripheral blood of 99 patients with ulcerative colitis (UC), 79 patients with Crohn's disease (CD), and 102 healthy controls. All participants were Japanese. SNPs at −656G/T, −607C/A, −137G/C, +113T/G, and +127C/T were determined by means of direct sequencing, and a genetic association with IBD was examined. The frequencies of the G allele at +113 and the T allele at +127 were significantly higher in patients with CD and UC compared with controls. The differences in allelic frequencies were more striking in patients with CD than in patients with UC, and at position +127 than at position +113. The haplotype estimation, according to the E-M algorithm, suggested that TACGT is closely associated with IBD, especially with CD. It was concluded that SNPs at the 5′-end of IL-18 gene might be closely related to the etiology of IBD.
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Citations
NLRP3 inflammasome and inflammatory bowel disease
TL;DR: The current literature regarding the physiology of NLRP3 inflammasome, mucosal immune response, and gut homeostasis as found in experimental models and IBD patients are reviewed.
IL-18 in autoimmunity: review
TL;DR: It is proposed that the disturbed mechanism of innate immunity, resulting from macrophage activation through innate immunity receptors (TLR/IL-1R family), may be the basis of pathologically high levels of IL-18 production and activation.
227
Molecular pathogenesis of inflammatory bowel disease: genotypes, phenotypes and personalized medicine.
TL;DR: The different loci implicated in disease risk are reviewed in the context of three proposed mechanisms leading to chronic inflammation of the gut mucosa: deregulation of the innate immune response to enteric microflora or pathogens; increased permeability across the epithelial barrier; and defective regulation of the adaptive immune system.
142
Local and systemic interleukin-18 and interleukin-18-binding protein in children with inflammatory bowel disease.
Steven T. Leach,Isabella Messina,Daniel A. Lemberg,Daniela Novick,Menachem Rubenstein,Andrew S. Day +5 more
TL;DR: IL‐18, produced in the colons of children with IBD, may contribute to local inflammatory changes and systemic IL‐18 level may be a useful indicator of gut inflammation.
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Interleukin-18 as a potential therapeutic target in chronic autoimmune/inflammatory conditions.
TL;DR: Evidence of its pro-inflammatory role in several human autoimmune and chronic inflammatory disorders; and data indicating that IL-18 blockade in animal models results in prevention/amelioration of the disease process and preservation of the target tissue integrity and function are focused on.
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References
Cloning and mutation analysis of the human IL-18 promoter: a possible role of polymorphisms in expression regulation.
TL;DR: The data indicate that common IL-18 promoter polymorphisms influence the expression ofIL-18 and potentially also of IFN-gamma.
487
Interleukin 18 is a primary mediator of the inflammation associated with dextran sulphate sodium induced colitis: blocking interleukin 18 attenuates intestinal damage
TL;DR: This article showed that IL-18 RNA levels increased very early in the colon during DSS-induced colitis in mice and IL18BP.Fc inhibited IBD associated weight loss and significantly inhibited the intestinal inflammation induced by DSS.
275
Crohn's disease in Japan: diagnostic criteria and epidemiology.
TL;DR: Clinically, Crohn's disease with only multiple small aphthous ulcerations, which is the earliest stage of the disease that is diagnosable, was found in 5 percent of patients.
217
•Journal Article
Regulation of IL-18 (IFN-gamma-inducing factor) gene expression.
TL;DR: The hypothesis that IL-18 expression may be coupled with apoptotic processes involving activation of ICE or ICE-like proteinase is proposed and expressed in a wide range of cell types.
176
Interleukin-18 Promoter Polymorphisms in Type 1 Diabetes
Adam Kretowski,Katarzyna Mironczuk,Anna Karpinska,Urszula Bojaryn,M Kinalski,Zbigniew Puchalski,Ida Kinalska +6 more
TL;DR: This study suggests the first evidence of an association between type 1 diabetes and polymorphisms in the promoter of IL-18 gene, and demonstrates that the contribution of -137GC genotypes to genetic susceptibility to type 1 Diabetes differs depending on the combination of IL -18 promotor gene haplotypes.
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