An association study between the Clara cell secretory protein CC16 A38G polymorphism and asthma phenotypes
Article first published online: 5 JUL 2002
Clinical & Experimental Allergy
Volume 32, Issue 7, pages 994–999, July 2002
How to Cite
Mansur, A. H., Fryer, A. A., Hepple, M., Strange, R. C. and Spiteri, M. A. (2002), An association study between the Clara cell secretory protein CC16 A38G polymorphism and asthma phenotypes. Clinical & Experimental Allergy, 32: 994–999. doi: 10.1046/j.1365-2222.2002.01426.x
- Issue published online: 5 JUL 2002
- Article first published online: 5 JUL 2002
- Submitted 31 August 2001; revised 26 October 2001; accepted 31 January 2002
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 ≤ 8 mg/mL) across the three genotypes. Homozygous individuals for the CC16*A allele did not demonstrate an increased risk of asthma when compared to heterozygous or GG homozygotes. In addition, no significant difference was observed in the distribution of the CC16*A or *G alleles in the asthmatics vs. non-asthmatics.
Conclusion CC16 polymorphism A38G does not influence the predisposition to asthma in this sample.