title: Association of three sets of high-affinity IgE receptor (FcepsilonR1) polymorphisms with aspirin-intolerant asthma.
abstract: OBJECTIVE
  The high-affinity IgE receptor comprises a tetramer of the ligand-binding alpha chain, a signal-augmenting beta chain, and a signal-transducing gamma chain dimer on mast cells. We hypothesized that the three subsets of the FCER1 gene may play a role in the development of the aspirin-intolerant asthma (AIA) phenotype and analyzed these genetic polymorphisms in association with clinical parameters in AIA patients.
  
  
  METHODS
  Six polymorphisms of FCER1 (FCERIA-344C>T, FCER1A-95T>C, MS4A2-109T>C, MS4A2 E237G, FCER1G-237A>G, FCER1G-54G>T) were genotyped in 126 AIA patients compared to 177 patients with aspirin-tolerant asthma (ATA) and 222 normal health controls (NC).
  
  
  RESULTS
  A significant difference in the genotype frequencies of FCER1G-237A>G was detected between AIA and ATA patients (p<0.05) both in co-dominant and recessive analysis models, whereas no significant relationships were identified between the frequencies of the other five single-nucleotide polymorphisms and AIA, ATA, and NC subjects. In addition, AIA patients carrying the homozygous AA genotype of FCER1G-237A>G exhibited significantly higher total serum IgE levels than did those with the GG/AG genotype (p=0.012). AIA patients expressing the CT/TT genotype at FCERIA-344C>T showed a higher prevalence of serum IgE specific to Staphylococcal enterotoxin A than did those with the CC genotype (p=0.008).
  
  
  CONCLUSIONS
  The FCER1G-237A>G and FCERIA-344C>T polymorphisms may contribute to the development of AIA in a Korean population.
authors.affiliation: Department of Allergy and Rheumatology, Ajou University School of Medicine, Suwon, South Korea.
authors.forename: Nami Shrestha
authors.initials: NS
authors.lastname: Palikhe
authors.forename: Seung-Hyun
authors.initials: SH
authors.lastname: Kim
authors.forename: Bo-Young
authors.initials: BY
authors.lastname: Cho
authors.forename: Young-Min
authors.initials: YM
authors.lastname: Ye
authors.forename: Gyu-Young
authors.initials: GY
authors.lastname: Hur
authors.forename: Hae-Sim
authors.initials: HS
authors.lastname: Park
mesh_terms: D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D000907:Antibodies, Bacterial / Q000097:blood; D001241:Aspirin / Q000009:adverse effects*; D001249:Asthma / Q000139:chemically induced / Q000235:genetics* / Q000276:immunology / Q000503:physiopathology; D001985:Bronchial Provocation Tests / Q000379:methods; D016022:Case-Control Studies; D005260:Female; D005541:Forced Expiratory Volume; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D017455:Receptors, IgE / Q000235:genetics*; D018089:Superantigens / Q000276:immunology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000907:Antibodies, Bacterial; D017455:Receptors, IgE; D018089:Superantigens; D007073:Immunoglobulin E; D001241:Aspirin