Recent physiological and pharmacological studies have indicated the po
tential importance of tryptase, the major protein component in mast ce
lls, in inflammatory diseases (especially asthma), Being released at i
nflammatory sites after the activation of mast cells, tryptase is capa
ble of causing bronchohyperresponsiveness and infiltration of eosinoph
ils, neutrophils, etc, in animal airways. The mechanisms by which tryp
tase causes bronchoconstriction involve probably the potentiation of o
ther chemical mediators such as histamine, production of bradykinin vi
a the hydrolysis of kininogen, and cleavage of the bronchodilating pep
tides VIP (vasoactive intestinal peptide) and PHM (peptide histidine-m
ethionine), Tryptase has also been found to be a potent mitogen in vit
ro for airway smooth muscle cells and epithelial cells, implying its r
ole in the hyperplasia of the asthmatic airways. The experimental data
providing evidence for the above roles of tryptase are summarized in
the present review, as well as the effects of tryptase inhibition in a
nimal asthma models, The potential strategies for the development of a
nti-asthmatic agents based on the inhibition of tryptase are discussed
.