Airway inflammation may contribute to the nonspecific bronchial hyperreactivity, which is a prominent feature in chronic asthma. Many stimuli such as allergens in allergic asthma, virus and irritants may induce an early reaction and in some cases a late reaction. An increase of nonspecific bronchial hyperreactivity is well demonstrated after this late reaction but no after the early one. Although a variety of inflammatory cells may be located within the respiratory tract, the late phase is generally considered as a direct consequence of the effects of mediators released from mast cells activated during the early reaction. Eosinophils and other inflammatory cells are attracted by chemotactic mediators such as PGD2. However the pathophysiology of chronic asthma remains uncertain because the heterogeneity of mast cells and the complexity of intercellular regulations. The role of basophils has been suggested mainly because their number increases during the late phase of allergic process. On the other hand, histamine and LTC4, but not PGD2, are found during the late phase: it is well established that basophils do not release PGD2. Two recent hypothesis have focused interest on basophils: the higher releasability property of basophils obtained from allergic and asthmatic patients, whatever their serum IgE and the presence of histamine releasing factors acting only on one kind of IgE (IgE+) which is apparently found in severe asthmatic patients. It may be probable that other cells, such as epithelial cells, play also a prominent role in chronic asthma.