Three groups of airway sensory nervous receptor may be involved in the pathophysiological changes in asthma and allergy. Those most active will be the C-fibre receptors, the rapidly adapting receptors, and A delta-nociceptive receptors. All are stimulated or sensitised by the inflammatory and immunological changes. The C-fibre receptors may mediate the axon reflex neurogenic inflammation-bronchoconstriction, mucus secretion and mucosal hyperaemia due to neuropeptide release-but the evidence for this process in humans, unlike rodents, is scanty. Activation of the receptors will also cause central nervous reflexes. The pathways for these reflexes in the brainstem, where their interactions, and the chemical neurotransmitters involved, are beginning to be delineated. The resulting reflexes include bronchoconstriction, mucus secretion and mucosal vasodilatation, responses that will amplify any similar changes due to neurogenic inflammation. The cough reflex depends on the interaction of the three basic reflex pathways. The reflexes show plasticity at peripheral, ganglionic and central nervous levels, and it is unlikely that results in acute experiments on healthy animals will apply quantitatively to humans with asthma.