Details

Autor(en) / Beteiligte

• Hollá, Lydie
• Văsku̇, Anna
• Znojil, Vladimír
• S̆is̆ková, Lenka
• Vácha, Jir̆í

Titel

Association of 3 gene polymorphisms with atopic diseases

Ist Teil von

• Journal of allergy and clinical immunology, 1999-04, Vol.103 (4), p.702-708

Ort / Verlag

New York, NY: Mosby, Inc

Erscheinungsjahr

1999

Quelle

Access via ScienceDirect (Elsevier)

Beschreibungen/Notizen

• Background: 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. 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 (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. Results: 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). Conclusion: It follows that the examined polymorphisms in the genes for ACE, angiotensinogen, and ET-1 could participate in the etiopathogenesis of atopic diseases. (J Allergy Clin Immunol 1999;103:702-8.)