Single nucleotide polymorphisms of the IL18 gene are associated with atopic eczema - 18/08/11
, Susanne Kruse, PhD b, Jana Potreck a, Laura Maintz, MD a, Claudia Jenneck a, Stephan Weidinger, MD c, Rolf Fimmers, PhD d, Thomas Bieber, MD, PhD a
Reprint requests: Natalija Novak, MD, Department of Dermatology, Sigmund-Freud-Str. 25, 53105 Bonn, Germany.Bonn, Hannover, and Munich, Germany
Abstract |
Background |
Human IL-18 is an inflammatory cytokine that plays a role in atopic diseases, such as atopic eczema (AE), by enhancing IL-4 and IL-13 production and stimulating the synthesis of IgE.
Objective |
To evaluate associations of polymorphisms in the IL18 gene on chromosome 11q22 with AE, we performed genotyping for single nucleotide polymorphisms (SNPs) in the IL18 gene in 225 patients with AE and 175 healthy control volunteers.
Methods |
Genotyping was performed by means of restriction fragment length polymorphism analysis.
Results |
Analyses revealed significant associations of SNPs +113[t/g] and +127[c/t] in exon 1, −137[g/c] in promoter region 1, and −133[c/g] in promoter region 2 with AE. These associations were not directly dependent on a specific subtype of AE or the concomitant manifestation of allergic rhinitis or asthma. On the functional level, the amount of IL-18 in the supernatants of PBMCs of patients with AE stimulated with Staphylococcus aureus enterotoxin B was significantly higher than that in healthy control subjects. In parallel, the amount of active IL-18 in the sera of patients with AE was enhanced at the exacerbation of their disease.
Conclusion |
In conclusion, our data suggest that SNPs in the IL18 gene might be involved in the development of AE by contributing to a functional dysregulation of the IL-18 production in vivo.
Le texte complet de cet article est disponible en PDF.Key words : IL-18, IgE, atopic eczema, allergy, polymorphism
Abbreviations used : AE, SEB, SNP
Plan
| Supported by grants from the Deutsche Forschungsgemeinschaft (DFG FOR NO/454-1-2 and DFG NO/454-2-1), the Herbert Reeck Stiftung of the University of Bonn, and BONFOR. |
Vol 115 - N° 4
P. 828-833 - avril 2005 Retour au numéro
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