Asthma as an axon reflex.
In asthma, damage to airway epithelium, possibly caused by eosinophil products, exposes C-fibre afferent nerve endings. Stimulation of these endings by inflammatory mediators such as bradykinin may result in an axon (local) reflex with antidromic conduction down afferent nerve collaterals and release of sensory neuropeptides such as substance P, neurokinin A, and calcitonin gene-related peptide. These peptides are potent inducers of airway smooth muscle contraction, bronchial oedema, extravasation of plasma, mucus hypersecretion, and possibly inflammatory cell infiltration and secretion. Thus, axon reflexes could account for at least some of the pathophysiology of asthma and this concept might lead to new strategies for treatment.
Barnes
P J
PJ
D001249:Asthma / Q000188:drug therapy / Q000503:physiopathology*; D001369:Axons / Q000502:physiology*; D004848:Epithelium / Q000502:physiology; D006801:Humans; D009419:Nerve Tissue Proteins / Q000378:metabolism; D012018:Reflex; D012137:Respiratory System / Q000294:innervation*; D011984:Sensory Receptor Cells / Q000502:physiology; D013373:Substance P / Q000378:metabolism
D009419:Nerve Tissue Proteins; D013373:Substance P