Excitatory non-adrenergic-non-cholinergic neuropeptides, such as the tachyk
inins substance P and neurokinin A, and its receptors are present in human
and animal airways. Tachykinins are biologically active at extremely low co
ncentrations. These peptides can cause potent inflammatory effects and can
affect airway function in a way that resembles features of asthma. Local re
lease of tachykinins affects blood vessels (vasodilatation and increased va
scular permeability) and bronchial smooth muscle (bronchoconstrition and hy
perresponsiveness). Neuropeptide research has revealed that tachykinins als
o play an important modulatory role in immune reactions. Tachykinins stimul
ate immune cells, such as mast cells, lymphocytes., and macrophages and are
chemotactic for neutrophils and eosinophils. Vice versa, a range of immune
cell mediators can also induce the release of tachykinins from excitatory
NANC nerve endings in the airways. In the last 20 years, significant advanc
es have been made in investigations of the interaction between immune cells
and nervous systems in chronic inflammatory diseases such as asthma. (C) 2
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