Two CD14 promoter polymorphisms and atopic phenotypes in Czech patients with IgE-mediated allergy
Article first published online: 19 SEP 2003
Volume 58, Issue 10, pages 1023–1026, October 2003
How to Cite
Bučková, D., Hollá, L. I., Schüller, M., Znojil, V. and Vácha, J. (2003), Two CD14 promoter polymorphisms and atopic phenotypes in Czech patients with IgE-mediated allergy. Allergy, 58: 1023–1026. doi: 10.1034/j.1398-9995.2003.00271.x
- Issue published online: 19 SEP 2003
- Article first published online: 19 SEP 2003
- Accepted for publication 21 April 2003
- allergic diseases;
- restriction fragment length polymorphism
Background: Immunoglobulin E (IgE)-mediated allergy belongs to common chronic disorders resulting from an interaction between both genetic and environmental factors. The gene encoding CD14 is a positional candidate gene for allergic diseases as it is localized on chromosome 5q31.1, a region that is linked to asthma and bronchial hyperresponsiveness. Recently, several polymorphisms in the promoter region of this gene have been associated with atopic phenotypes in various populations.
Methods: We investigated relationship among atopic phenotypes and two polymorphisms [C(-159)T and G(-1359)T] in the promoter of the CD14 gene in the Czech population. Polymerase chain reaction with restriction fragment length polymorphism analyses was used to determine the CD14 genotypes in subjects with IgE-mediated allergic diseases (n = 562) and random controls (n = 320).
Results: The CD14 allele or genotype distributions were similar in patients and control group. However, the frequency of the C allele of the C(-159)T polymorphism was higher in patients with positive skin prick tests for moulds than in patients without reactivity to this antigen (P < 0.002, Pcorr<0.01). In addition, we found that patients with homozygous genotype (GG) of the G(-1359)T polymorphism had marginally lower percentage of positive skin prick tests compared with the other genotypes (P < 0.029, Pcorr > 0.05).
Conclusions: Our study supports the idea that CD14 gene variants may act as disease modifiers of IgE-mediated allergic diseases.