title: beta2 adrenoceptor Arg16Gly polymorphism, airway responsiveness, lung function and asthma in infants and children.
abstract: BACKGROUND
  We have previously reported a relationship between increased airway responsiveness (AR) in infancy and reduced childhood lung function.
  
  
  OBJECTIVE
  The current study aimed to determine whether the Arg16Gly polymorphism of the beta2 adrenoceptor (beta2AR) gene was important to this relationship.
  
  
  METHODS
  A cohort that initially numbered 253 individuals underwent assessments of AR and lung function aged 1 month, 6 and 11 years; genotyping for polymorphisms of the beta(2)AR was performed.
  
  
  RESULTS
  At 1 month of age, the genotype homozygous Arg16 (n=24) was associated with a mean increase in log dose-response slope (AR) of 0.27 [95% confidence interval (CI) 0.07, 0.49] compared with the genotype homozygous Gly16 (n=58), P=0.01. At 11 years of age, the genotype homozygous Arg16 (n=35) was associated with a mean reduction in the percentage of forced expiratory volume in 1 s of 5.3% [95% CI 0.3, 10.2] compared with the genotype homozygous Gly16 (n=65), P=0.03. There was no association between the Arg16Gly polymorphism and atopy or diagnosed asthma. However, nine of 69 individuals with the genotype homozygous Gly16 were admitted to hospital with asthma compared with five out of 111 individuals with the remaining genotypes (P<0.05).
  
  
  CONCLUSIONS
  The Arg16Gly polymorphism may be important to the association between increased AR in infancy and reduced lung function in childhood and may also be a determinant of asthma severity in children but not asthma per se.
authors.affiliation: School of Paediatrics and Child Health, University of Western Australia, Perth, Australia. s.w.turner@abdn.ac.uk
authors.forename: S W
authors.initials: SW
authors.lastname: Turner
authors.forename: S-K
authors.initials: SK
authors.lastname: Khoo
authors.forename: I A
authors.initials: IA
authors.lastname: Laing
authors.forename: L J
authors.initials: LJ
authors.lastname: Palmer
authors.forename: N A
authors.initials: NA
authors.lastname: Gibson
authors.forename: P
authors.initials: P
authors.lastname: Rye
authors.forename: L I
authors.initials: LI
authors.lastname: Landau
authors.forename: J
authors.initials: J
authors.lastname: Goldblatt
authors.forename: P N
authors.initials: PN
authors.lastname: Le Souëf
mesh_terms: D001249:Asthma / Q000235:genetics* / Q000503:physiopathology*; D016535:Bronchial Hyperreactivity; D001985:Bronchial Provocation Tests; D002648:Child; D005260:Female; D005838:Genotype; D006801:Humans; D006967:Hypersensitivity / Q000235:genetics / Q000503:physiopathology; D007223:Infant; D016015:Logistic Models; D008168:Lung / Q000503:physiopathology*; D008297:Male; D011110:Polymorphism, Genetic; D011446:Prospective Studies; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics*; D018709:Statistics, Nonparametric
chemical_list: D018343:Receptors, Adrenergic, beta-2