Neurogenic inflammation and asthma

Abstract

The release of neurotransmitters may exacerbate the inflammatory response. Such neurogenic inflammation has been documented in a number of inflammatory diseases. Neurogenic inflammation due to release of neuropeptides from sensory nerves has been demonstrated in airways of several species, particularly rodents, and may contribute to the inflammatory response in asthmatic airways. Tachykinins (substance P and neurokinin A) released from airway sensory nerves may cause bronchoconstriction, vasodilatation, plasma exudation, and mucus secretion, whereas another sensory neuropeptide, calcitonin generelated peptide, may contribute to hyperemia of inflammation. Airway epithelial damage in asthma exposes sensory nerves which may become sensitized by inflammatory products (including prostaglandins and cytokines) so that neuropeptides are released via a local reflex trigger such as bradykinin, resulting in exaggerated inflammation. The effects of tachykinins may be amplified further by loss of the major degrading enzyme, neutral endopeptidase, from epithelial cells. Direct evidence for neurogenic inflammation in asthma is still awaited, however. Several strategies for reducing neurogenic inflammation are possible, particularly inhibition of neuropeptide release from sensory nerves by stimulating prejunctional receptors such as mu-opioid receptors.