Matsuo Muneaki, Sasaki Kazuya, Ichimaru Tomohiro, Nakazato Sachie, Hamasaki Yuhei
Department of Pediatrics, Faculty of Medicine, Saga University, Saga, Japan.
Pediatr Neurol. 2006 Aug;35(2):102-6. doi: 10.1016/j.pediatrneurol.2005.12.005.
This study examined the possibility that children with and without a history of febrile seizures might mount different immune responses to double-stranded ribonucleic acid, which is a common viral factor that induces host cell immune responses, and is recognized by Toll-like receptor 3. The production of interleukin-1beta and interferon-alpha from double-stranded ribonucleic acid-stimulated leukocytes was examined in 27 children (age 3.6+/-0.3 years) with a history of febrile seizures and in 18 children (age 3.4+/-0.2 years) without a history of febrile seizures. Significantly (P=0.0007) increased interleukin-1beta production was observed in children with a history of febrile seizures, compared with control subjects. When patients with a single prior episode of febrile seizures (n=9) and those with multiple prior episodes of febrile seizures (n=18) were compared, a significant difference in interleukin-1beta production was not observed. Genotyping of interleukin-1beta(-511), Toll-like receptor 3, Toll-IL-1 receptor domain-containing adapter inducing interferon-beta, and interleukin-1 receptor antagonist polymorphisms revealed no significant differences in allelic distribution among febrile seizure patients and control subjects. Interleukin-1beta production was not significantly influenced by genotype. Viral infection results in increased interleukin-1beta production in febrile seizure patients, and this may play a role in febrile seizures.
本研究探讨了有或无热性惊厥病史的儿童对双链核糖核酸是否会产生不同免疫反应的可能性。双链核糖核酸是一种常见的病毒因子，可诱导宿主细胞免疫反应，并可被Toll样受体3识别。我们检测了27名有热性惊厥病史的儿童（年龄3.6±0.3岁）和18名无热性惊厥病史的儿童（年龄3.4±0.2岁）经双链核糖核酸刺激的白细胞产生白细胞介素-1β和干扰素-α的情况。与对照组相比，有热性惊厥病史的儿童白细胞介素-1β的产生显著增加（P = 0.0007）。比较单次热性惊厥发作史的患者（n = 9）和多次热性惊厥发作史的患者（n = 18），未观察到白细胞介素-1β产生的显著差异。白细胞介素-1β（-511）、Toll样受体3、含Toll-IL-1受体结构域的衔接蛋白诱导干扰素-β和白细胞介素-1受体拮抗剂多态性的基因分型显示，热性惊厥患者与对照组之间等位基因分布无显著差异。白细胞介素-1β的产生不受基因型的显著影响。病毒感染导致热性惊厥患者白细胞介素-1β产生增加，这可能在热性惊厥中起作用。
