Mucus Trafficking through the Laryngopharynx
IgE-mediated histamine liberation, in conjunction with other
inflammatory mediators, precipitates mucosal oedema, augmented mucus
secretion, bronchial smooth muscle constriction, and airway
architectural alterations in both the nasal and bronchopulmonary
regions[34, 37-40]. Enhanced mucus translocation from
the bronchi or nasal cavity towards the larynx may instigate epithelial
irritation, compromise glottic closure, and provoke airway reflexive
responses, culminating in a diverse array of aerodigestive
manifestations[25, 41]. Although post-nasal drip (PND)
is posited as a pivotal component of the UACS hypothesis, its
attribution as the aetiological agent for symptoms such as throat
clearing and cough in patients with AR and ARS remains a subject of
academic debate, especially when nasoendoscopic observations do not
corroborate anomalous secretions[26]. Additionally, the UACS
paradigm may be insufficient in addressing the multifaceted
symptomatology accompanying or occurring independently of cough in UTCS.
Nasal Airflow Obstruction
Nasal congestion in AR leads to a compensatory shift towards oral
respiration, bypassing the nasal humidification and filtration
mechanisms. This change may undermine the laryngopharyngeal epithelial
barrier by promoting mucosal desiccation, increasing allergen deposition
in the aerodigestive tract, and exacerbating lower airway constriction
[28].
Secondary Phonotrauma
Phonotrauma, often linked to vocal misuse or overuse[42].,
refers to epithelial damage induced by excessive vocal cord vibrations
or contact[43] [44]. Chronic airway symptoms such
as persistent cough and throat clearing, which necessitate robust
laryngeal contraction and elevated glottic pressure, can secondarily
induce phonotrauma[44]. This may initiate a self-sustaining
feedback loop of irritation and reflexive symptoms over time, as
depicted in Figure 2 [45] [46].
United Airway effects
A growing corpus of literature advocates for the ”Unified Airway Model,”
in which different segments of the respiratory tract are considered as
functionally interconnected[40, 47, 48].
Inflammatory mediators, specifically vascular cytokines, circulate
locally, enabling inflammation in one segment to influence others. While
this concept has been well-studied in the context of lower airway and
nasal interactions[29, 39, 48], its
implications for the laryngopharynx remain largely unexplored yet offer
a plausible mechanism linking nasal and lower airway inflammation with
non-specific chronic laryngitis.