Inflammation and coagulation are complex biological pathways that interact with each other in a variety of chronic diseases. Although they are often considered to be distinct processes, it is almost impossible to dissect the one from the other, except at their functional extremes.1 Activation of the coagulation cascade appears to be common to diverse inflammatory lung diseases such as acute lung injury, idiopathic lung fibrosis, acute respiratory distress syndrome and sarcoidosis.2 It is no great surprise, then, to find evidence of activation of the coagulation cascade in a chronic inflammatory disease such as asthma. Indeed, several studies over the last 10 years or so have consistently found markers for coagulation in the airways of subjects with asthma.3 4 5 6 7 However, taking an informative snapshot of all the relevant team members in coagulation and inflammation in such a setting is a bit like taking a photograph of a 10-car pile-up on a motorway. Such pictures could generate widespread speculation as to the true course of events that led to the disaster. A comprehensive exploration of the presence of various factors governing the balance between coagulation and fibrinolysis, and their relationship to asthma severity has been lacking. In this issue of Thorax, Brims et al (see page 1037) provide a new, more complete montage of the potential family members of the coagulation cascade present in the asthmatic airway.8 What can we learn from it, and what future work would help us see how inflammatory pile-ups may be modulated or prevented?

Although glucocorticosteroids are the mainstay of asthma treatment, many of the structural changes that occur in the airways appear to be steroid resistant.9 10 …