Pawlik A, Kaminski M, Kuśnierczyk P, Kurzawski M, Dziedziejko V, Adamska M, Safranow K, Gawronska-Szklarz B
Department of Pharmacokinetics and Therapeutic Drug Monitoring, Pomeranian Medical University, ul.Polst.Wlkp. 72, 70-111 Szczecin, Poland.
Tissue Antigens. 2007 Oct;70(4):314-8. doi: 10.1111/j.1399-0039.2007.00908.x.
Allergic asthma is a chronic inflammatory disease in which interleukin-18 (IL-18) plays an important role. However, there are controversial reports on IL-18 promoter polymorphism as an independent marker of asthma susceptibility. The aim of the present study was to examine the IL-18 promoter polymorphism in patients with allergic asthma. Two hundred and thirty-one patients with allergic asthma from a Polish population diagnosed according to the National Heart, Lung, and Blood Institute (NHLBI)/WHO guidelines were examined. An allele-specific polymerase chain reaction was used to analyse polymorphisms at positions -137 and -607 in the promoter region of the IL-18 gene. Neither in the -607 C>A nor in the -137 G>C promoter polymorphism were there any differences observed between the total group of asthmatic patients and the controls in the frequencies of genotypes, alleles, diplotypes or haplotypes. In patients with severe asthma, the -607 CC and -137 GG genotypes were observed significantly more frequently (P = 0.03 for both), whereas in patients with mild and moderate asthma, the -137 CC genotype was more prevalent than in the former group. The strongest difference between mild to moderate and severe asthma was observed in -137 allele frequencies (P = 0.006). The results of the present study suggest that the -137 G allele and the C-G/C-G diplotype seem to be involved in the pathogenesis of the severe form of asthma.
过敏性哮喘是一种慢性炎症性疾病,其中白细胞介素-18(IL-18)发挥着重要作用。然而,关于IL-18启动子多态性作为哮喘易感性独立标志物的报道存在争议。本研究的目的是检测过敏性哮喘患者的IL-18启动子多态性。对根据美国国立心肺血液研究所(NHLBI)/世界卫生组织(WHO)指南诊断的231名波兰过敏性哮喘患者进行了检测。采用等位基因特异性聚合酶链反应分析IL-18基因启动子区域-137和-607位点的多态性。在-607 C>A和-137 G>C启动子多态性中,哮喘患者总体与对照组在基因型、等位基因、双倍体型或单倍体型频率上均未观察到差异。在重度哮喘患者中,-607 CC和-137 GG基因型的观察频率显著更高(两者P均=0.03),而在轻度和中度哮喘患者中,-137 CC基因型比前一组更普遍。在-137等位基因频率上观察到轻度至中度哮喘与重度哮喘之间的差异最为显著(P = 0.006)。本研究结果表明,-137 G等位基因和C-G/C-G双倍体型似乎参与了重度哮喘的发病机制。