Eosinophils are strongly implicated as a major proinflammatory cell in the pathogenesis of asthma. Basic proteins from the crystalloid granule may be responsible for damage to mucosal epithelium whereas membrane-derived lipid mediators (particularly platelet activating factor and leukotriene C4) might directly influence bronchial smooth muscle contraction, microvascular permeability and mucus hypersecretion. The numbers of eosinophils and their products correlated with the severity of disease whereas successful treatment is usually associated with a resolution of local eosinophilia. Neutrophils may also be implicated in the pathogenesis of asthma but the evidence that this cell per se plays an important role remains controversial. Neutrophil products have the potential for altering airway function. More research is required to define the precise role of this cell type in asthma. It needs to be emphasised that the inflammation associated with bronchial asthma is complex and involves several cell types (i.e. T lymphocytes, mast cells and macrophages) in addition to the eosinophil and neutrophil.