Genetic variants of FcepsilonRIbeta and Il-4 and atopy in a Polish population.
BACKGROUND
Atopy results from the interaction between genetic and environmental factors. The aim of our study was to clarify the association between the FcRIint2 polymorphic variant, the Glu237Gly mutation in exon 7 of FcepsilonRIbeta and (-590 C/T) Il-4 gene promoter polymorphism with atopy in a randomized Polish sample.


METHODS
Unrelated subjects aged 18-45 years who were residents of an urban area (Lodz, Poland) were included in the study: 98 patients with asthma and/or allergic rhinitis, and 87 non-atopic, non-asthmatic controls. We used common criteria for atopy and asthma. Atopic status was determined by positive skin prick tests (SPT) and IgE levels. The severity of asthma was assessed in spirometric measurements; SPTs to house dust mite (HDM) and mixed grass pollen (MGP) were performed. Total and specific IgE were measured in each subject. Genotypic analysis was performed by PCR for FcRIint2 and (590 C/T) Il-4 gene promoter polymorphism and ARMS-PCR was performed for the Glu237Gly mutation.


RESULTS
We found a statistically significant association between atopy and FcRIint2 variant polymorphism (OR = 2.96), a correlation between positive skin prick tests to MGP and raised MGP-specific IgE concentrations in patients bearing this variant (OR = 4.0). We did not observe that the FcRIint2 variant was associated with positive SPTs to HDM or high levels of HDM-specific IgE (OR = 1.0). The intronic variant of FcepsilonRIbeta was strongly correlated with elevated total serum IgE (OR = 4.74). No statistically significant association was found between atopy and the Glu237Gly mutation of FcepsilonRIbeta(OR = 1.36) or (-590 C/T) Il-4 gene promoter polymorphism (OR = 0.88).


CONCLUSIONS
The results suggest that FcRIint2 polymorphism is related to atopy and may influence its development.
Korzycka-Zaborowska
B
B
Department of Pneumonology and Allergy, Medical University of Lódz', Poland. barbara_korzycka@op.pl
Hopkin
J M
JM
Górski
P
P
D000293:Adolescent; D000328:Adult; D019943:Amino Acid Substitution; D001249:Asthma / Q000453:epidemiology / Q000235:genetics; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000453:epidemiology / Q000235:genetics*; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D015847:Interleukin-4 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020125:Mutation, Missense; D017354:Point Mutation; D011044:Poland / Q000453:epidemiology; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics; D017455:Receptors, IgE / Q000235:genetics* / Q000502:physiology; D012221:Rhinitis, Allergic, Perennial / Q000453:epidemiology / Q000235:genetics; D006255:Rhinitis, Allergic, Seasonal / Q000453:epidemiology / Q000235:genetics; D012882:Skin Tests
D017455:Receptors, IgE; D015847:Interleukin-4; D007073:Immunoglobulin E