In recent years, the emerging concept of bronchial inflammation as a prominent
histopathologic characteristic of asthma has profoundly modified the view of the role of the
mast cell, which was traditionally thought to be linked to the release of soluble chemical
mediators substantially involved in the genesis of acute, immediate bronchospasm. The
finding that the production of proinflammatory cytokines by mast cells in asthmatic airways is
comparable, in some circumstances, to that of T-cell origin, has led to the hypothesis that …