Eosinophilic inflammation has long been considered one of the most distinctive pathological hallmarks of asthma¹ and features in many contemporary definitions of this disease. A plethora of studies published from the mid 1990s onwards have suggested, however, that airway eosinophilia is not a universal finding. This has fuelled debate that discrete pathological phenotypes of asthma may exist, with the neutrophil—rather than the eosinophil—dominating in certain circumstances.^2–4 We present data that support the current renewed interest in the neutrophil as a primary driver of airways inflammation, particularly in the most severe forms of asthma. There are also some intriguing data to suggest that, when the eosinophil has been “red carded” and disappears from the inflamed airway, the neutrophil may be drawn in and act as the substitute granulocyte.

The hypothesis that the eosinophil is the key effector cell involved in the pathogenesis of asthma has run into trouble for several reasons: (1) eosinophilic inflammation is present in the airway lumen of only 50% of asthmatic subjects;⁴ (2) even intense eosinophilic inflammation, as occurs in eosinophilic bronchitis, fails to induce asthma;⁵ (3) many asthma exacerbations occur …