Abstract
ObjectiveOlfaction is impaired in chronic rhinosinusitis (CRS). The study has two aims: (1) to determine whether changes in cation concentration occur in the olfactory mucus of mice with CRS, which may affect chemo-electrical transduction, (2) and to examine whether these alterations are physiologically significant in humans.Study DesignAnimal study in mice and translational study in humans.MethodsInflammation was induced by sensitization and chronic exposure of 16 C57BL/6 mice to Aspergillus fumigatus. The control group included 16 untreated mice. Ion-selective microelectrodes were used to measure free cation concentrations in the olfactory mucus of 8 mice from each treatment group, while the remaining mice were sacrificed for histology. To validate the findings in the animal model, olfactory threshold was measured in 11 healthy human participants using Sniffin’ Sticks before and after nasal irrigation with solutions that were composed of either of the cation concentrations.ResultsIn 8 mice, olfactory mucus of chronically inflamed mice had lower [Na+] (84.8±4.45 mM versus 93.73±3.06 mM, p = 0.02), and higher [K+] (7.2±0.65 mM versus 5.7±0.20 mM, p = 0.04) than controls. No difference existed in [Ca2+] (0.50±0.12 mM versus 0.54±0.06 mM, p = 0.39). In humans, rinsing with solutions replicating ion concentrations of the mouse mucosa with chronic inflammation caused a significant elevation in the median olfactory threshold (9.0 to 4.8, p = 0.003) but not with the control solution (8.3 to 7.8, p = 0.75).ConclusionChronic inflammation elevates potassium and lowers sodium ion concentration in mice olfactory mucus. Nasal irrigation with a corresponding solution induced olfactory threshold shift in humans.
Highlights
Chronic rhinitis and rhinosinusitis affect approximately 33 million people in the United States and are primary etiologies for olfactory loss among patients [1]
One result of inflammation may be a change in the ion concentration of the olfactory mucus, which could potentially interfere with the olfactory sensory neurons (OSNs) chemo-electrical signal transduction process and olfaction
Histology and Immunohistochemistry Sensitized animals chronically exposed to A. fumigatus showed dense inflammatory infiltrates in many areas of the respiratory epithelium and mild inflammation in the olfactory epithelium
Summary
Chronic rhinitis and rhinosinusitis affect approximately 33 million people in the United States and are primary etiologies for olfactory loss among patients [1]. The mechanisms by which rhinitis and rhinosinusitis cause olfactory dysfunction are likely multifactorial and include direct effects of inflammatory mediators on olfactory sensory neurons (OSNs) in addition to respiratory mucosal edema and reduced airflow to the olfactory cleft [2]. The olfactory cleft is rich in OSNs within the olfactory epithelium that project sensory cilia into the nasal cavity and are bathed in a specialized mucus layer. These cilia are rich in membrane-bound G-protein coupled odorant-binding receptor proteins [3].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
