Kuo Chou Tsai-Nung, Li Ying-Shiuan, Lue Ko-Huang, Liao Che-Feng, Lin Chien-Yu, Tzeng Pei-Rung, Wong Ruey-Hong
Institute of Medicine, College of Health Care and Management, Chung-Shan Medical University Hospital, Taichung, Taiwan.
J Asthma. 2010 Jun;47(5):532-8. doi: 10.3109/02770901003686472.
Cellular defenses against allergens and reactive oxygen species (ROS) exposure are critical in the pathogenesis of asthma. CD14 is a receptor for various bacterial products, such as lipopolysaccharides (LPS), and is also a mediator of inflammatory processes. Manganese superoxide dismutase (MnSOD) is an ROS scavenger, and myeloperoxidase (MPO) can convert hydrogen peroxide into hypochlorous acid; thus, they are considered to be involved in inflammatory defense. The authors conducted a case-control study to evaluate the susceptibility to childhood asthma based on CD14, MnSOD, and MPO genes.
The CD14 -260, MnSOD -9, and MPO -463 genotypes were identified by polymerase chain reactions for 116 asthmatic children and 232 healthy controls. Questionnaires were administered to obtain demographic characteristics. Allergen testing used common Taiwanese aeroallergens.
A higher level of parental education, family history of asthma, incense burning at home, allergen-test positive, and the MnSOD Val-Ala/Ala-Ala genotypes (matched relative risk = 2.0; 95% confidence interval = 1.0-4.2) were significantly associated with childhood asthma. Interactions between CD14, MnSOD, MPO genotypes and allergy status were significantly associated with asthma risk in these children (all p <.001). Furthermore, atopic cases with MnSOD Val-Ala/Ala-Ala (log eosinophil 2.66/mm(3), log total serum immunoglobulin E [IgE] 2.48 IU/ml) or Val-Val (log eosinophil 2.61/mm(3), log total serum IgE 2.63 IU/ml) genotypes had elevated eosinophil counts and total serum IgE levels as compared to nonatopic cases with MnSOD Val-Val genotype (log eosinophil 2.27/mm(3), log total serum IgE 1.83 IU/ml).
Susceptible MnSOD genotypes might modulate the development of asthma in Taiwanese children.
细胞对抗变应原和活性氧(ROS)暴露的防御在哮喘发病机制中至关重要。CD14是多种细菌产物(如脂多糖,LPS)的受体,也是炎症过程的介质。锰超氧化物歧化酶(MnSOD)是一种ROS清除剂,髓过氧化物酶(MPO)可将过氧化氢转化为次氯酸;因此,它们被认为参与炎症防御。作者进行了一项病例对照研究,以评估基于CD14、MnSOD和MPO基因的儿童哮喘易感性。
通过聚合酶链反应对116例哮喘儿童和232例健康对照进行CD14 -260、MnSOD -9和MPO -463基因型鉴定。发放问卷以获取人口统计学特征。变应原检测使用常见的台湾空气变应原。
较高的父母教育水平、哮喘家族史、家中焚香、变应原检测阳性以及MnSOD Val-Ala/Ala-Ala基因型(匹配相对风险=2.0;95%置信区间=1.0-4.2)与儿童哮喘显著相关。CD14、MnSOD、MPO基因型与过敏状态之间的相互作用与这些儿童的哮喘风险显著相关(所有p<.001)。此外,与MnSOD Val-Val基因型的非特应性病例(对数嗜酸性粒细胞2.27/mm³,对数总血清免疫球蛋白E[IgE]1.83 IU/ml)相比,MnSOD Val-Ala/Ala-Ala(对数嗜酸性粒细胞2.66/mm³,对数总血清IgE 2.48 IU/ml)或Val-Val(对数嗜酸性粒细胞2.61/mm³,对数总血清IgE 2.63 IU/ml)基因型的特应性病例嗜酸性粒细胞计数和总血清IgE水平升高。
易感性MnSOD基因型可能调节台湾儿童哮喘的发生发展。