Tracheobronchial sensory C-fiber

Tracheobronchial sensory C-fibers are a population of unmyelinated, slow-conducting afferent nerve fibers that innervate the airways and lungs[1][3][4]. They are a subtype of vagal sensory fibers, often referred to as bronchopulmonary C-fibers or airway sensory C-fibers, and mediate responses to a wide variety of chemical, thermal, and mechanical stimuli present in the airway, including irritants (e.g., capsaicin, acid, pollutants), endogenous mediators (e.g., bradykinin, prostaglandins, cytokines), and infectious agents[2][3][4][7][9]. Activation of these sensory fibers by such stimuli can result in pronounced respiratory and cardiovascular reflexes, including bronchoconstriction, increased airway mucus secretion, cough, tachypnea, bradycardia, and hypotension[1][6][8]. They are key contributors to the sensation of airway irritation or discomfort in conditions like asthma and viral respiratory infections (such as COVID-19), and are involved in both protective and pathological airway reflexes[3][7][9]. Due to their nature as a *functional population of neurons* rather than a discrete molecular entity (e.g., receptor, enzyme, ion channel), "Tracheobronchial sensory C-fiber" is not considered a canonical therapeutic target per se; rather, the molecular receptors expressed by these fibers (such as TRPV1, TRPA1, bradykinin B2, adenosine A1/A2a) are the direct actionable targets for drug interventions[2][6].

Other names

Bronchopulmonary C-fiberVagal C-fiberC-fiber nociceptorAirway sensory C-fiberBronchopulmonary C-fiber afferentCFR (C-fiber receptor)Group C nerve fiber

Activation or desensitization of ion channels (TRPV1, TRPA1), GPCR-mediated responses (bradykinin B2 receptor, adenosine A1/A2a receptors), Modulation of excitability by inflammatory mediators