Asthma exacerbation by aspirin and chemical additives: use of a nucleotide template model to investigate potential mechanisms.

Aspirin exacerbated asthma (AEA) affects approximately 10% of the asthmatic population. Clinical studies with a focus on abnormalities in arachidonate metabolism do not adequately account for susceptibility. Other pharmacological targets of aspirin receive less attention. Further investigation is required to elucidate mechanisms, improve on diagnosis and treatment. This study employs a molecular modeling approach, based on use of a nucleotide template, to standardise and compare molecular structures of compounds known to induce or prevent asthma. Results identify relative molecular similarity within the structures of drugs and cell mediators relevant to AEA and intolerance reactions. The investigated compounds provide equivalent fits to ligand structures for GABA, glycine, NMDA and nicotinic receptors. Chloride and ligand-gated ion channels are a common link between agents responsible for the induction and control of AEA. The methodology is applicable to compounds responsible for chemical-induced intolerance reactions..