Association of 3 gene polymorphisms with atopic diseases

Background: Various peptidases, including angiotensin-converting enzyme (AC E), inactivate some inflammatory peptides that are considered to influence the pathogenesis of atopic diseases. This enzyme is also involved in the co nversion or activation of 2 bronchoconstriction mediators: angiotensin II f rom angiotensinogen and endothelin (ET), respectively. Objective: We tested a hypothesis that asthma or other atopic diseases are associated with insertion/deletion ACE, M235T angiotensinogen, and TaqI ET- 1 gene polymorphisms, Methods: A case-control approach was used in the study, Healthy subjects (1 41 persons) were used as control subjects, and 231 patients with histories of atopic asthma, allergic rhinitis, atopic dermatitis, or a combination th ereof were studied. ACE genotype was determined by PCR, angiotensinogen M23 5T and ET-1 by PCR, and restriction analysis by AspI and TaqI, respectively , Results: We Found the significant association of the insertion/deletion pol ymorphism of the ACE, as well as that of M235T polymorphism of the angioten sinogen genes, with the group of patients with atopic diseases (P =.0025 an d P =.0204, respectively). No difference was proved for the intron 4 (posit ion 8000) polymorphism in the ET-1 gene when comparing the atopic patients with the control group (P =.1774), A significant difference was found betwe en groups of patients with both asthma and rhinitis and patients without bo th respiratory atopic diseases (P =.0033). Conclusion: It follows that the examined polymorphisms in the genes for ACE , angiotensinogen, and ET-1 could participate in the etiopathogenesis of at opic diseases.