Question special

Thank you for your interesting points about the mechanism of eosinophils in COPD exacerbation. It was noted that neither trial reported triggers of exacerbation. Would we expect there to be a difference in anti-IL5 effect based upon the type of exacerbation? Can we biologically define eosinophilic vs. non-eosinophilic exacerbations? It seems a biomarker for COPD exacerbation itself is key to finding the subpopulation that anti-IL5 therapy would have the greatest benefit in.