Tachykinins and neuro-immune interactions in asthma.

Excitatory non-adrenergic-non-cholinergic neuropeptides, such as the tachykinins substance P and neurokinin A, and its receptors are present in human and animal airways. Tachykinins are biologically active at extremely low concentrations. These peptides can cause potent inflammatory effects and can affect airway function in a way that resembles features of asthma. Local release of tachykinins affects blood vessels (vasodilatation and increased vascular permeability) and bronchial smooth muscle (bronchoconstrition and hyperresponsiveness). Neuropeptide research has revealed that tachykinins also play an important modulatory role in immune reactions. Tachykinins stimulate 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 advances have been made in investigations of the interaction between immune cells and nervous systems in chronic inflammatory diseases such as asthma.