title: The polymorphisms of Eotaxin 1 and CCR3 genes influence on serum IgE, Eotaxin levels and mild asthmatic children in Taiwan.
abstract: BACKGROUND
  Asthma is a complex disorder, which is known to be affected by interactions between genetic and environmental factors. The human Eotaxin 1 and CCR3 attract eosinophils and Th2-lymphocytes to migrate to the inflammatory foci that could represent a key mechanism in allergy and asthma.
  
  
  OBJECTIVE
  We hypothesized that Eotaxin1 gene Ala23Thr and A-384 G, and CCR3 gene T51C polymorphisms are associated with plasma Eotaxin levels and predispose individuals to asthma pathogenesis.
  
  
  METHODS
  One hundred seventy-eight hospital-based asthmatic children and 277 community-based controls aged from 5 to 12 years were recruited in southern Taiwan. Whole blood samples and questionnaires were collected. In this study, we addressed genetic effects of Eotaxin 1 and CCR3 genes on asthma, plasma IgE and Eotaxin 1 levels.
  
  
  RESULTS
  In comparison with subjects with Ala23Ala genotype, Ala23Thr polymorphism of the Eotaxin 1 gene showed a significant protective effect on asthma (AOR = 0.58, 95% CI = 0.37-0.92). We demonstrated that the mean Eotaxin 1 concentration was significantly higher in subjects with Ala23Ala than in subjects with Thr23Thr (P = 0.005) or Ala23Thr (P = 0.07), which showed a gene-dose dependent relationship. But, we observed that the A-384G polymorphism of Eotaxin 1 gene and T51C polymorphism of CCR3 gene are not associated with asthma.
  
  
  CONCLUSIONS
  This study finding provide a strong evidence that Eotaxin 1 Thr23Thr homozygote has a protective effect on asthma and significantly decreases plasma Eotaxin 1 concentrations in asthmatics in Taiwan.
authors.affiliation: Faculty of Public Health, Kaohsiung Medical University, Kaohsiung, Taiwan.
authors.forename: T-N
authors.initials: TN
authors.lastname: Wang
authors.forename: W
authors.initials: W
authors.lastname: Chiang
authors.forename: H-I
authors.initials: HI
authors.lastname: Tseng
authors.forename: Y-T
authors.initials: YT
authors.lastname: Chu
authors.forename: W-Y
authors.initials: WY
authors.lastname: Chen
authors.forename: N-H
authors.initials: NH
authors.lastname: Shih
authors.forename: Y-C
authors.initials: YC
authors.lastname: Ko
mesh_terms: D001249:Asthma / Q000235:genetics* / Q000276:immunology*; D054413:Chemokine CCL11 / Q000097:blood* / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D004247:DNA / Q000097:blood / Q000302:isolation & purification; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism; D005260:Female; D005787:Gene Frequency / Q000276:immunology; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D008297:Male; D011110:Polymorphism, Genetic / Q000235:genetics* / Q000276:immunology; D012150:Polymorphism, Restriction Fragment Length / Q000235:genetics / Q000276:immunology; D020641:Polymorphism, Single Nucleotide / Q000235:genetics / Q000276:immunology; D054397:Receptors, CCR3 / Q000235:genetics* / Q000378:metabolism; D012016:Reference Values; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D013624:Taiwan
chemical_list: D054413:Chemokine CCL11; D054397:Receptors, CCR3; D007073:Immunoglobulin E; D004247:DNA