title: Association of asthma and the interleukin-4 promoter gene in Japanese.
abstract: BACKGROUND
  Susceptibility to the development of asthma and other atopic diseases is known to be associated with genetic components. Several investigator have linked the interleukin-4 (IL-4) gene and nearby markers located on chromosome 5 to atopy and asthma. Recent study has demonstrated that the T allele of a polymorphism in the IL-4 gene promoter region (C-590T) is associated with elevated levels of total serum IgE.
  
  
  OBJECTIVE
  The objective of this study was to evaluate the possible role of this IL-4 polymorphism (C-590T) in modulating the allergic response and asthma in Japanese children.
  
  
  RESULTS
  The study was conducted in two different populations: families ascertained through asthmatic children (asthmatic group, 306 members) in whom linkage of asthma and atopy to chromosome 5q31-33 is suggested and a random general population (control group, 215 members). The IL-4 C-590T polymorphism was genotyped by PCR-restriction fragment length polymorphism analysis. Frequency of the T allele was 0.73 in the asthmatic group and 0.70 in the control group. No significant difference in the levels of total serum IgE and specific IgE to house dust mite was observed between subjects with homozygote for the C allele, a heterozygote and a homozygote for the T allele by intrafamilial and interfamilial comparisons. Using the transmission disequilibrium test, however, we found a significantly frequent transmission of the T allele to asthmatic children (chi2=5.72, P=0.023).
  
  
  CONCLUSIONS
  Our data suggest that the IL-4 promoter C-590T polymorphism may be associated with the development of asthma in Japanese children, but not through modulating total serum IgE levels.
authors.affiliation: Department of Paediatrics, Institute of Clinical Medicine, University of Tsukuba, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Noguchi
authors.forename: M
authors.initials: M
authors.lastname: Shibasaki
authors.forename: T
authors.initials: T
authors.lastname: Arinami
authors.forename: K
authors.initials: K
authors.lastname: Takeda
authors.forename: Y
authors.initials: Y
authors.lastname: Yokouchi
authors.forename: T
authors.initials: T
authors.lastname: Kawashima
authors.forename: H
authors.initials: H
authors.lastname: Yanagi
authors.forename: A
authors.initials: A
authors.lastname: Matsui
authors.forename: H
authors.initials: H
authors.lastname: Hamaguchi
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000818:Animals; D000906:Antibodies / Q000097:blood; D001249:Asthma / Q000097:blood / Q000453:epidemiology / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D005260:Female; D005787:Gene Frequency; D005796:Genes / Q000235:genetics*; D005838:Genotype; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D015847:Interleukin-4 / Q000235:genetics*; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D008925:Mites / Q000276:immunology; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics
chemical_list: D000906:Antibodies; D015847:Interleukin-4; D007073:Immunoglobulin E