Etiology and pathology of prolonged cough

Abstract

 Cough is a biological defense reaction, and its pathway has physiological response and pathological reaction.

 As a pathological reaction, there are states of increased or decreased cough sensitivity, in addition these cough receptors mediated mechanisms are stimulated by mechanically or chemically, C-fiber receptors are stimulated by airway inflammation and the neuropeptides such as substance P (SP), neurokinin A (NK-A) and CGRP are released, especially it is believed that SP stimulates receptors in Aδ fibers and its impulse is transmitted via the vagal nerve afferent pathway to the medullary cough center, and causing coughing.

 There is other mechanism via smooth muscle contraction in pathological cough reaction, and each of which is independent.

 Prolonged cough is thought to be due to either pathway of two pathological responses or merger of both pathways.

 On the other hand, TRPV1 cloned as a capsaicin receptor is expressed in sensory nerve specific (C fiber, Aδ fiber).

 Our study showed that TRPV1 was distributed in all respiratory organs and co-localized with SP, NK-A and CGRP.

 It is suggest that TRPV1 is involved in cough and airway contraction because these neuropeptides are released from it by stimulation, in addition it is thought that its activation could be more hypersensitive due to airway inflammation.