Asthma is a complex disorder characterized by paroxysmal airways constriction, an increased responsiveness of the airways to inhaled spasmogens, and an eosinophilic inflammatory infiltrate. Increases in prevalence and in mortality and morbidity rates have been observed within the past 2 decades. Although the factors that have contributed to this observed increase are not completely apparent, genetic influences such as parental atopy, air pollution, modernization of life style, viral or bacterial exposure in early childhood, allergen exposure, and diet have all been implicated.

It has become apparent that even when asymptomatic, many asthmatics have abnormal airway function and a degree of airways inflammation, with the T lymphocyte a pivotal cell type involved in the pathophysiology of asthma (Figure 1). Moreover, the presence of inflammatory cells, particularly T cells and eosinophils, within the lungs of asthmatic individuals is coordinated by the local release of cytokines. These small glycosylated proteins are involved in communication among all the cells of the immune system implicate in asthma (lymphocytes, eosinophils, mast cells, and basophils) as well as between these cells and structural cells (epithelial cells, endothelial cells, smooth muscle cells, fibroblasts). This article reviews current knowledge regarding the histopathology of asthma, with specific reference to the inflammatory cells and cytokines that are attracting particular interest.