Scientific Community - Aims and Hypotheses


  1. To phenotype children attending secondary care asthma clinics in Scotland
  2. To establish a clinical database
  3. To establish a biobank for storage of DNA collected from asthmatic children
  4. To study hypothesis driven gene-environment interactions within a population of asthmatic children in Scotland using a case-only design. Candidate genes will be the Arg16Gly polymorphism of the beta 2 adrenoceptor, filaggrin and antioxidant genes GSTTM and GSTTP. Environmental factors will include exposure to environmental tobacco smoke and dietary vitamin E intake.

Research Questions

  1. Are asthmatic children with genetically determined susceptibility to antioxidant stress and who are exposed to environmental oxidants (including tobacco smoke and dietary vitamin E) more likely to be non-atopic?
  2. What is the overall burden of filaggrin null mutations in Scottish asthmatic children? do these children represent a particularly difficult to treat subgroup and are they particularly vulnerable to individual environmental insults?
  3. Is bronchodilator response (BDR) attenuated in asthmatic children with homozygous genotype Arg16 and is this exaggerated by treatment with long acting beta agonists and palliated by treatment with leukotriene receptor antagonists?