Hollá L, Văsků A, Znojil V, Sisková L, Vácha J
Institute of Pathological Physiology, Medical Faculty, Masaryk University Brno, Czech Republic.
J Allergy Clin Immunol. 1999 Apr;103(4):702-8. doi: 10.1016/s0091-6749(99)70246-0.
Various peptidases, including angiotensin-converting enzyme (ACE), inactivate some inflammatory peptides that are considered to influence the pathogenesis of atopic diseases. This enzyme is also involved in the conversion or activation of 2 bronchoconstriction mediators: angiotensin II from angiotensinogen and endothelin (ET), respectively.
We tested a hypothesis that asthma or other atopic diseases are associated with insertion/deletion ACE, M235T angiotensinogen, and TaqI ET-1 gene polymorphisms.
A case-control approach was used in the study. Healthy subjects (141 persons) were used as control subjects, and 231 patients with histories of atopic asthma, allergic rhinitis, atopic dermatitis, or a combination thereof were studied. ACE genotype was determined by PCR, angiotensinogen M235T and ET-1 by PCR, and restriction analysis by AspI and TaqI, respectively.
We found the significant association of the insertion/deletion polymorphism of the ACE, as well as that of M235T polymorphism of the angiotensinogen genes, with the group of patients with atopic diseases ( P =.0025 and P =.0204, respectively). No difference was proved for the intron 4 (position 8000) polymorphism in the ET-1 gene when comparing the atopic patients with the control group (P =.1774). A significant difference was found between groups of patients with both asthma and rhinitis and patients without both respiratory atopic diseases (P =.0033).
It follows that the examined polymorphisms in the genes for ACE, angiotensinogen, and ET-1 could participate in the etiopathogenesis of atopic diseases.
多种肽酶，包括血管紧张素转换酶（ACE），可使一些被认为影响特应性疾病发病机制的炎性肽失活。该酶还分别参与两种支气管收缩介质的转化或激活：即从血管紧张素原生成血管紧张素II和内皮素（ET）。
我们检验了一个假设，即哮喘或其他特应性疾病与ACE基因的插入/缺失多态性、M235T血管紧张素原多态性以及TaqI内皮素-1基因多态性相关。
本研究采用病例对照法。健康受试者（141人）作为对照，研究了231例有特应性哮喘、过敏性鼻炎、特应性皮炎病史或其组合的患者。ACE基因型通过聚合酶链反应（PCR）测定，血管紧张素原M235T和内皮素-1分别通过PCR及AspI和TaqI酶切分析测定。
我们发现ACE基因的插入/缺失多态性以及血管紧张素原基因的M235T多态性与特应性疾病患者组显著相关（分别为P = 0.0025和P = 0.0204）。比较特应性患者与对照组时，ET-1基因第4内含子（位置8000）多态性未发现差异（P = 0.1774）。哮喘和鼻炎患者组与无两种呼吸道特应性疾病的患者组之间存在显著差异（P = 0.0033）。
由此可见，ACE、血管紧张素原和ET-1基因中检测到的多态性可能参与了特应性疾病的发病机制。
