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Am. J. Respir. Crit. Care Med., Volume 161, Number 1, January 2000, 124-127

Association between Plasma CC16 Levels, the A38G Polymorphism, and Asthma

INGRID A. LAING, CEDRIC HERMANS, ALFRED BERNARD, PAUL R. BURTON, JACK GOLDBLATT, and PETER N. LE SOUËF

Department of Paediatrics, University of Western Australia, Children's Hospital Medical Centre, Perth, Australia; Unit of Industrial Toxicology and Occupational Medicine, Faculty of Medicine, Catholic University of Louvain, Brussels, Belgium; Division of Biostatistics and Genetic Epidemiology, TVW Telethon Institute for Child Health Research, West Perth, Australia; and Genetic Services, Princess Margaret Hospital for Children, Perth, Australia

The effect of the A38G polymorphism on Clara cell secretory protein (CC16) gene expression and asthma was investigated by measuring plasma CC16 levels in 100 asthmatic and nonasthmatic children. Restriction digestion determined the A38G genotype and plasma CC16 levels were analyzed using a sensitive latex immunoassay. Asthmatics had lower mean plasma CC16 levels adjusted for age and gender (7.96 µg/L; 95% confidence interval [CI] = 6.79 to 9.31) than nonasthmatic subjects (9.98 µg/L; 95% CI = 8.83 to 11.26) (p = 0.006). Similarly adjusted, mean plasma CC16 levels were also lower in 38A/38A (6.79 µg/L; 95% CI = 4.56 to 9.02) than 38G/38G subjects (10.01 µg/L; 95% CI = 7.90 to 12.12; p = 0.003). The odds ratio for asthma diagnosis of 38A/38A subjects was 4.78 (95% CI = 1.08 to 21.18; p = 0.04) compared with 38G/38G subjects. However, this was reduced when corrected from plasma CC16 level, suggesting that the odds of asthma was largely mediated through altered plasma CC16 levels. The 38A sequence was associated with reduced plasma CC16 levels and individuals with lower plasma CC16 levels were more likely to have asthma. This provides further evidence for a significant role of the CC16 gene, 38A allele in the development of asthma. Laing IA, Hermans C, Bernard A, Burton PR, Goldblatt J, Le Souëf PN. Association between plasma CC16 levels, the A38G polymorphism, and asthma.




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