Given our recent observation that secondary bacterial infections occurred in 60% of COPD subjects following experimental rhinovirus infection, and that virus-induced neutrophilic airway inflammation was implicated in precipitating bacterial overgrowth via neutrophil elastase-mediated degradation of anti-microbial peptides, therapeutic approaches that reduce neutrophil migration and activation might have the attractive potential of preventing secondary bacterial infections [7]. This evidence concerns the gene ELANE and inflammatory response.