Original Paper

Association Analysis of Tyrosine Kinase FYN Gene Polymorphisms in Asthmatic Children
Aleksandra Szczepankiewicz^{a, b}, Anna Brborowicz^a, Maria Skibiska^b, Monika Wiko^c, Marta Tomaszewska^c, Joanna Hauser<sup>b

a</sup>Department of Pediatric Pulmonology, Allergy and Clinical Immunology, 3rd Department of Pediatrics and
^bLaboratory of Psychiatric Genetics, Department of Psychiatry, Poznan University of Medical Sciences, Poznan, and
^cClinical Neuropsychology Unit, Nicolaus Copernicus University Torun, Collegium Medicum Bydgoszcz, Bydgoszcz, Poland

Address of Corresponding Author

Int Arch Allergy Immunol 2008;145:43-47 (DOI: 10.1159/000107465)

  Key Words

• Asthma
• FYN tyrosine kinase gene
• Polymorphism

  Abstract

Background: FYN is nonreceptor tyrosine kinase that represents the earliest detectable signaling response after antigen-activated inflammatory cells. Studies in animal models of allergic asthma have shown that inhibitors of tyrosine kinases exert an anti-inflammatory effect. In the FYN gene, several polymorphisms have been described. There have, however, been no studies analyzing the impact of FYN gene polymorphisms on the course and severity of asthma. The aim of this study was to analyze the possible relationship between three polymorphisms (-93A/G, Intron10+37C/T and Ex12+894T/G) in the FYN gene and asthma. Methods: We analyzed 120 pediatric asthmatic patients aged from 6 to 18 years. The diagnosis of allergic asthma was based on clinical manifestation, lung function test and positive skin prick tests and/or an increased IgE level. The control group consisted of 187 healthy subjects. The polymorphisms were genotyped with use of the PCR-RFLP method. Results: We observed an association of the -93A/G polymorphism and the presence of asthma (p = 0.014 for genotypes and p = 0.019 for alleles) and in the subgroup of 55 patients with severe asthma (p = 0.042 for genotypes and p = 0.021 for alleles). We also found an association of the Ex12+894T/G polymorphism in the whole group analyzed (p = 0.067 for genotypes and p = 0.024 for alleles), but not in the subgroup with severe asthma. For the Intron10+37T/C polymorphism, we did not find a significant difference between the whole group of asthmatic patients and the control group nor between the subgroup with severe asthma and the control group. In the linkage disequilibrium analysis, we observed a modest linkage between -93A/G and Intron10+37T/C polymorphisms (lod = 18.7, D' = 0.62, 95% CI: 0.51-0.71, r² = 0.29); however, it was not strong enough to generate any haplotypes. Conclusions: The results may suggest a relationship between the FYN polymorphisms and allergic asthma.

Copyright © 2007 S. Karger AG, Basel

  Author Contacts

Correspondence to: Dr. Aleksandra Szczepankiewicz
Department of Pediatric Pneumonology, Allergy and Clinical Immunology
Poznan University of Medical Sciences
27/33 Szpitalna St., PL-60-572 Poznan (Poland)
Tel. +48 61 849 1311, Fax +48 61 848 0111, E-Mail alszczep@amp.edu.pl

  Article Information

Received: November 20, 2006
Accepted after revision: June 18, 2007
Published online: August 17, 2007
Number of Print Pages : 5
Number of Figures : 0, Number of Tables : 1, Number of References : 18