Polymorphism of angiotensin I converting enzyme (ACE) gene according to the severity of asthma in Korean adult asthmatics

Kim, Mi Kyeong; Bae, Jang Whan

Abstract

BACKGROUND AND OBJECTIVE
Many chemical mediators such as histamine, prostaglandins, leukotrienes, bradykinin, angiotensisn II (A II), and even angiotensin converting enzyme (ACE) affect the pathophysiology of asthma. ACE exists in the epithelium, endothelium, neuroepithelium, plasma, and especially in high concentrations in human lung tissue. ACE converts A I to A II, which is highly vasoconstrictive, bronchoconstrictive, inflammatory substance, and can also inactivate bradykinin. ACE polymorphism determines the level of ACE such as DD, higher concentration of ACE, but II, lowest concentration of that, so in DD type, the level of A II increase, but that of bradykinin decrease. From that point we can speculate polymorphism of ACE gene anyhow affects asthma, so we carried out this study for evaluating relationships between the ACE genotype distribution and genesis and severity of asthma in Korean adult asthmatics.
MATERIALS AND METHODS
The study population consisted of 150 asthmatics, 57 patients of non asthmatic lung diseases including lung cancer (n=10), pulmonary tuberculosis (n=27), empyema (n=3), pneumonia (n=11), bronchiectasis (n=5) and lung abscess (n=1) and 100 normal healthy subjects without hypertension, cardiovascular disease, diabetes mellitus and nephropathy which may bias the result. Bronchial asthmatics were classified into 3 groups according to the criteria of the NAPE. PCR (polymerase chain reaction) for ACE genotypes was performed. PCR products were electrophoresed in 1% agarose gels, and then DNA pattern was directly visualized under ethidium bromide staining.
RESULTS
The frequency for II, ID, and DD genotypes were 46 (46%), 38 (38%), 16 (16%) in control group, 59 (39.6%), 74 (49.5%), 17 (10.9%) in asthma group and 28 (49.1%), 24 (42.1%), 5 (8.8%) in non-bronchial lung disease group, respectively. There was no signi- ficant difference in frequency of ACE genotype distribution among the 3 groups (p > 0.05). The frequency for II, ID, and DD genotypes in the 3 groups of asthmatics were 17 (34%), 27 (54%), 6 (12%) in mild subset, 13 (26%), 30 (60%), 7 (14%) in moderate subset, and 11 (22%), 33 (66%), 6 (12%) in severe subset. Even though there was also no significant difference among the 3 severity subsets in the asthma group, the frequency of non-DD subsets such as II and ID was higher in moderate and severe asthmatics.
CONCLUSION
The results suggest that ACE gene polymorphism dose not affect the genesis but can progress asthma in Korean adult asthmatics. However, further mass studies on asthmatics will be needed to clarify the effect of ACE polymorphism on the severity of Korean adult asthmatics.