Abstract
Angiotensin-Converting enzyme (ACE) inactivates bradykinin, substance P, and neurokinin A, which are thought to play important roles in the pathogenesis of inflammatory diseases. Expression of angiotensinogen, a precursor of angiotensin, is enhanced by augmented secretion of proinflammatory cytokines (eg, interleukin-1) in the site of inflammation. Insertion or deletion (I/D) ACE and M235T angiotensinogen gene polymorphisms were reported to be associated with atopy in a Czech population. Using polymerase chain reaction restriction fragment length polymorphism and SNaPshot typing analysis, we investigated the frequencies of the genotypes and alleles of the ACE gene in 137 patients with allergic rhinitis, of the M235T angiotensinogen gene in 186 patients with allergic rhinitis, and of both in 219 healthy control subjects. There was no difference in the frequency of the DD genotype of the ACE gene in the controls and patients (odds ratio, 1.32 [0.66–2.60]; p > .05). The D allele was more frequent in patients, but the difference was not statistically significant (odds ratio, 1.21 [0.89–1.64]; p > .05). There was no difference in the frequency of the TT genotype of the angiotensinogen gene in the controls and patients (odds ratio, 1.01 [0.38–2.69]; p > .05). The T allele was more frequent in patients, but the difference was not statistically significant (odds ratio, 1.10 [0.78–1.55]; p > .05). Our results indicate that polymorphisms in the genes for ACE and angiotensinogen may not be related to the development of allergic rhinitis in the Korean population.
Get full access to this article
View all access options for this article.