Asthma is characterized by inflammation, hyperresponsiveness, and remodelin
g of the airway. Human mast cells (HMCs) play a central role in all of thes
e changes by releasing mediators that cause exaggerated bronchoconstriction
, induce human airway smooth muscle (HASM) cell proliferation, and recruit
and activate inflammatory cells. Moreover, the number of HMCs present on as
thmatic HASM is increased compared with that on nonasthmatic HASM. HASM cel
ls also have the potential to actively participate in the inflammatory proc
ess by synthesizing cytokines and chemokines and expressing surface molecul
es, which have the capacity to perpetuate the inflammatory mechanisms prese
nt in asthma. This review specifically examines how the mediators of HMCs h
ave the capacity to modulate many functions of HASM; how the synthetic func
tion of HASM, particularly through the release and expression of stem cell
factor, has the potential to influence HMC number and activation in an extr
aordinarily potent and proinflammatory manner; and how these interactions b
etween HMCs and HASM have potential consequences for airway structure and i
nflammation relevant to the disease process of asthma.