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Abstract：
BACKGROUND: Lichen planus (LP) is a chronic inflammatory disease with uncertain etiology. Interleukin-18 (IL-18) is an interferon gamma (INFγ) inducing agent. It is a pro-inflammatory cytokine that was found to play a role in the pathogenesis of some autoimmune disorders.
METHODS: This study included 50 patients with classic cutaneous lichen planus (CLP) and 50 healthy volunteers serving as controls. Venous blood samples were withdrawn from the study subjects under complete aseptic precautions. Blood samples were examined for single nucleotide polymorphisms (SNPs) of IL-18 gene at promoter -137(G/C) and -656 (G/T) using polymerase chain reaction (PCR) and IL-18 level was assessed using enzyme linked immunosorbent assay (ELISA).
RESULTS: The mean level of IL-18 was significantly higher in CLP patients (31.63 ± 4.90) compared to control subjects (13.95 ± 6.82). Significantly high levels of IL-18 were found among patients with diabetes, hypertension (p < 0.01 in both). HCV positive patients and patients with both OLP and CLP also expressed higher levels of IL-18. Genotypic and allelic distribution at position -137(G/C) showed that the genotype GG was present at significantly higher frequency in cases (58%) compared to controls (28.0%). On the other hand the CC genotype at position -137 was significantly higher in the controls (28%) as compared to CLP cases (6%). Polymorphism of IL-18 at position -656(G/T) showed no significant difference between cases and controls. No significant difference could be detected in IL-18 level between different genotypic variants at position -137(G/C) and -656(G/T).
CONCLUSIONS: IL-18 may play important role in pathogenesis of LP. Elevated IL-18 levels could be part of the pro-inflammatory autoimmune process in LP. The presence of OLP, HCV, diabetes and hypertension is associated with higher production of IL-18. IL-18 promotor region -137(G/C) polymorphism might be a factor that increase the risk of development of lichen planus in Egyptian patients.
METHODS: This study included 50 patients with classic cutaneous lichen planus (CLP) and 50 healthy volunteers serving as controls. Venous blood samples were withdrawn from the study subjects under complete aseptic precautions. Blood samples were examined for single nucleotide polymorphisms (SNPs) of IL-18 gene at promoter -137(G/C) and -656 (G/T) using polymerase chain reaction (PCR) and IL-18 level was assessed using enzyme linked immunosorbent assay (ELISA).
RESULTS: The mean level of IL-18 was significantly higher in CLP patients (31.63 ± 4.90) compared to control subjects (13.95 ± 6.82). Significantly high levels of IL-18 were found among patients with diabetes, hypertension (p < 0.01 in both). HCV positive patients and patients with both OLP and CLP also expressed higher levels of IL-18. Genotypic and allelic distribution at position -137(G/C) showed that the genotype GG was present at significantly higher frequency in cases (58%) compared to controls (28.0%). On the other hand the CC genotype at position -137 was significantly higher in the controls (28%) as compared to CLP cases (6%). Polymorphism of IL-18 at position -656(G/T) showed no significant difference between cases and controls. No significant difference could be detected in IL-18 level between different genotypic variants at position -137(G/C) and -656(G/T).
CONCLUSIONS: IL-18 may play important role in pathogenesis of LP. Elevated IL-18 levels could be part of the pro-inflammatory autoimmune process in LP. The presence of OLP, HCV, diabetes and hypertension is associated with higher production of IL-18. IL-18 promotor region -137(G/C) polymorphism might be a factor that increase the risk of development of lichen planus in Egyptian patients.
摘要：
背景：扁平苔藓（LP）是一种病因不确定的慢性炎症性疾病。白细胞介素-18(IL-18)是干扰素γ(IFNγ)诱导剂。它是一种促炎细胞因子，被发现在某些自身免疫性疾病的发病机理中起作用。
方法：本研究包括50例典型皮肤扁平苔藓（CLP）患者和50例健康志愿者作为对照。在完全无菌预防措施下从研究对象中抽取静脉血样。使用聚合酶链反应（PCR）检查血液样品中IL-18基因在启动子-137（G/C）和-656（G/T）的单核苷酸多态性（SNP），并使用酶联免疫吸附测定（ELISA）评估IL-18水平。
结果：CLP患者的IL-18平均水平（31.63±4.90）明显高于对照组（13.95±6.82）。在糖尿病患者中发现显著高水平的IL-18,高血压(两者p<0.01)。HCV阳性患者和患有OLP和CLP的患者也表达更高水平的IL-18。位置-137（G/C）的基因型和等位基因分布表明，与对照组（28.0％）相比，病例（58％）的基因型GG以明显更高的频率存在。另一方面,与CLP病例(6%)相比,对照(28%)中位置-137处的CC基因型显著更高。IL-18在位置-656（G/T）的多态性在病例和对照组之间没有显着差异。在位置-137(G/C)和-656(G/T)的不同基因型变体之间,在IL-18水平中没有检测到显著差异。
结论：IL-18可能在LP的发病机制中起重要作用。IL-18水平升高可能是LP促炎自身免疫过程的一部分。OLP的存在,HCV,糖尿病和高血压与更高的IL-18产生有关。IL-18启动子区-137（G/C）多态性可能是增加埃及患者扁平苔藓发展风险的因素。
方法：本研究包括50例典型皮肤扁平苔藓（CLP）患者和50例健康志愿者作为对照。在完全无菌预防措施下从研究对象中抽取静脉血样。使用聚合酶链反应（PCR）检查血液样品中IL-18基因在启动子-137（G/C）和-656（G/T）的单核苷酸多态性（SNP），并使用酶联免疫吸附测定（ELISA）评估IL-18水平。
结果：CLP患者的IL-18平均水平（31.63±4.90）明显高于对照组（13.95±6.82）。在糖尿病患者中发现显著高水平的IL-18,高血压(两者p<0.01)。HCV阳性患者和患有OLP和CLP的患者也表达更高水平的IL-18。位置-137（G/C）的基因型和等位基因分布表明，与对照组（28.0％）相比，病例（58％）的基因型GG以明显更高的频率存在。另一方面,与CLP病例(6%)相比,对照(28%)中位置-137处的CC基因型显著更高。IL-18在位置-656（G/T）的多态性在病例和对照组之间没有显着差异。在位置-137(G/C)和-656(G/T)的不同基因型变体之间,在IL-18水平中没有检测到显著差异。
结论：IL-18可能在LP的发病机制中起重要作用。IL-18水平升高可能是LP促炎自身免疫过程的一部分。OLP的存在,HCV,糖尿病和高血压与更高的IL-18产生有关。IL-18启动子区-137（G/C）多态性可能是增加埃及患者扁平苔藓发展风险的因素。
