Abstract
Purpose of ReviewDespite their high prevalence, the pathophysiology of allergic rhinitis (AR) and chronic rhinosinusitis (CRS) remains unclear. Recently, transient receptor potential (TRP) cation channels emerged as important players in type 2 upper airway inflammatory disorders. In this review, we aim to discuss known and yet to be explored roles of TRP channels in the pathophysiology of AR and CRS with nasal polyps.Recent FindingsTRP channels participate in a plethora of cellular functions and are expressed on T cells, mast cells, respiratory epithelial cells, and sensory neurons of the upper airways. In chronic upper airway inflammation, TRP vanilloid 1 is mostly studied in relation to nasal hyperreactivity. Several other TRP channels such as TRP vanilloid 4, TRP ankyrin 1, TRP melastatin channels, and TRP canonical channels also have important functions, rendering them potential targets for therapy.SummaryThe role of TRP channels in type 2 inflammatory upper airway diseases is steadily being uncovered and increasingly recognized. Modulation of TRP channels may offer therapeutic perspectives.
Highlights
Rhinitis and rhinosinusitis represent two clinical entities of chronic upper airway diseases, characterized by inflammationThis article is part of the Topical Collection on RhinosinusitisConsidering rhinitis, three major phenotypes can be recognized and distinguished: allergic rhinitis (AR), infectious rhinitis, and the heterogenous group of non-allergic rhinitis (NAR) [2]
Edema, mucus production, and—in the case of CRSwNP—nasal polyp formation lead to nasal obstruction, whereas rhinorrhea and postnasal drip are the result of mucus production and often impaired mucociliary clearance [4–6]
In Europe, up to 30% and over 10% of the general population suffers from AR [9] and chronic rhinosinusitis (CRS) respectively [10], which comes with an enormous socio-economic impact [11–14]
Summary
Rhinitis and rhinosinusitis represent two clinical entities of chronic upper airway diseases, characterized by inflammation. Considering rhinitis, three major phenotypes can be recognized and distinguished: allergic rhinitis (AR), infectious rhinitis, and the heterogenous group of non-allergic rhinitis (NAR) [2]. In case of chronic rhinosinusitis (CRS), a phenotype with (CRSwNP) and without nasal polyps (CRSsNP) can be distinguished [3]. In Europe, both AR and CRSwNP feature mainly type 2 inflammatory processes. Edema, mucus production, and—in the case of CRSwNP—nasal polyp formation lead to nasal obstruction, whereas rhinorrhea and postnasal drip are the result of mucus production and often impaired mucociliary clearance [4–6]. In AR, allergens can cause nasal itch and sneezing through binding of histamine to its receptor on afferent
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