Peripheral airway C-fiber sensory nerve

Peripheral airway C-fiber sensory nerves are unmyelinated afferent neurons that play a critical role in protecting the respiratory system by detecting noxious stimuli (Mazzone & Undem, 2016). These fibers originate primarily from the jugular and nodose ganglia of the vagus nerve and terminate in the airway epithelium and mucosa (Undem & Taylor-Clark, 2014). Upon activation by chemical irritants, inflammatory mediators, or mechanical stress, they release proinflammatory neuropeptides such as Substance P and Calcitonin Gene-Related Peptide (CGRP), leading to neurogenic inflammation, bronchoconstriction, and mucus hypersecretion (Lee & Pisarri, 2001). In pathological conditions like chronic cough, asthma, and COPD, these nerves often exhibit hypersensitivity, contributing to persistent symptoms (Canning et al., 2014). Therapeutic strategies targeting these fibers focus on modulating specific ion channels, such as P2X3 or TRPV1, to inhibit the initiation of sensory signals and alleviate airway hyperresponsiveness (Belvisi & Birrell, 2017). Additionally, blocking the receptors for the neuropeptides they release, such as Neurokinin-1 receptors, has been explored to mitigate downstream inflammatory effects (Joos et al., 2000).

Other names

Bronchial C-fiberPulmonary C-fiberVagal C-fiber afferentNociceptive airway afferentAirway nociceptorAirway C-fiber afferent

Inhibition of sensory nerve activation and signal conduction through the antagonism of excitatory ion channels (e.g., P2X3, TRPV1) or the modulation of voltage-gated sodium channels, as well as the blockade of downstream neuropeptide receptors (e.g., NK1), to reduce the cough reflex and neurogenic inflammation.