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An association study between the Clara cell secretory protein CC16 A38G polymorphism and asthma phenotypes
A H Mansur1, A A Fryer, M Hepple
1Lung Injury & Inflammation Group, Department of Respiratory Medicine, Keele University and North Staffordshire Hospital, Staffordshire, UK. adelmansur@hotmail.com
Background:
Previously, an association has been reported between an increased risk of asthma and a polymorphism in the Clara cell secretory protein (CC16) gene [namely, an adenine to guanine substitution in the CC16 gene at position 38 (A38G) downstream from the transcription initiation site within the noncoding region of exon 1]. Homozygous individuals for the polymorphic sequence (AA genotype) were reported to have a significant (6.9 fold) increased risk of developing asthma. This finding has not been confirmed independently.
Objective:
To validate the association of CC16 A38G polymorphism to asthma in a separate well-characterized population through a case-control study.
Methods:
We conducted an association study using a sample of 217 unrelated Northern European Caucasians. Individuals were clinically characterized by a validated respiratory questionnaire, spirometry and bronchial reactivity measurement, and genotyped for the A38G polymorphism using PCR and restriction digestion. Association analysis was performed using the nonparametric Chi-squared tests.
Results:
In the unselected population, 43.3% participants were homozygous for the CC16*G allele and 45.4% were heterozygous (AG). We observed no significant difference in the distribution of positive bronchial reactivity to methacholine (at FEV1 PC20 of
Conclusion:
CC16 polymorphism A38G does not influence the predisposition to asthma in this sample.