Fatal attacks of asthma are usually associated with obstruction of the airways with mucus (mucus plugs). During his postdoctoral fellowship in the Erle lab, Luke Bonser found that mucus plugs were heterogeneous, with some areas that contained one type of mucus glycoprotein (MUC5AC) and other areas containing a different one (MUC5B). Using airway epithelial cells from human donors provided by our collaborators Walt Finkbeiner and Lorna Zlock, Luke went on to show that he could model mucus plugs in cell cultures stimulation with the central asthma mediator, interleukin-13 (IL-13). Whereas mucus in the cultures was readily transported by ciliated cells in unstiumulated cultures, IL-13 stimulation almost completely eliminated mucus transport. Luke showed that this was due not to abnormalities in ciliated cell function, but instead to the attachment, or tethering, of IL-13-induced MUC5AC to the epithelium. The work was published in the Journal of Clinical Investigation and highlighted as a "Scientific Showstopper" by the JCI editors.