Airway sensory C-fiber (C-fiber)

Airway sensory C-fibers are unmyelinated, slow-conducting afferent nerve fibers that originate in the vagal ganglia and terminate in the airway mucosa and parenchyma (Mazzone & Undem, 2016). They serve as a primary defense mechanism, responding to chemical irritants, inflammatory mediators (such as bradykinin and prostaglandins), and mechanical stimuli to trigger protective reflexes like coughing and bronchoconstriction (Lee & Pisarri, 2001). In chronic respiratory diseases such as asthma, COPD, and chronic cough, these fibers often become hypersensitive or 'hyperexcitable,' leading to exaggerated responses to otherwise innocuous stimuli (Chung, 2014). Therapeutic interventions targeting these fibers aim to suppress this hypersensitivity by inhibiting specific receptors (e.g., P2X3, TRPV1) or blocking signal conduction, thereby reducing symptoms and neurogenic inflammation (Morice et al., 2021). While effective in reducing cough, targeting these fibers requires careful consideration of the protective role they play in preventing aspiration and clearing the airways.

Other names

Bronchopulmonary C-fiberPulmonary C-fiberVagal C-fiberNociceptive airway afferent

Pharmacological modulation of airway sensory C-fibers typically involves the antagonism of specific ion channels (e.g., P2X3, TRPV1, TRPA1) or the blockade of voltage-gated sodium channels to reduce neuronal firing and the subsequent release of pro-inflammatory neuropeptides (Mazzone & Undem, 2016; Morice et al., 2021).