title: Association of 3 gene polymorphisms with atopic diseases.
abstract: 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).
  
  
  CONCLUSIONS
  It follows that the examined polymorphisms in the genes for ACE, angiotensinogen, and ET-1 could participate in the etiopathogenesis of atopic diseases.
authors: Institute of Pathological Physiology, Medical Faculty, Masaryk University Brno, Czech Republic.
authors: L
authors: L
authors: Hollá
authors: A
authors: A
authors: Văsků
authors: V
authors: V
authors: Znojil
authors: L
authors: L
authors: Sisková
authors: J
authors: J
authors: Vácha
mesh_terms: D000293:Adolescent; D000328:Adult; D000483:Alleles; D000808:Angiotensinogen / Q000235:genetics*; D001249:Asthma / Q000235:genetics; D016022:Case-Control Studies; D003876:Dermatitis, Atopic / Q000235:genetics; D019332:Endothelin-1 / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020125:Mutation, Missense; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D017354:Point Mutation; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic; D015183:Restriction Mapping; D006255:Rhinitis, Allergic, Seasonal / Q000235:genetics
chemical_list: D019332:Endothelin-1; D000808:Angiotensinogen; D007703:Peptidyl-Dipeptidase A