Anosmia, the loss of smell, is a common and often the sole symptom of COVID-19. The onset of the sequence of pathobiological events leading to olfactory dysfunction remains obscure. Here, we have developed a postmortem bedside surgical procedure to harvest endoscopically samples of respiratory and olfactory mucosae and whole olfactory bulbs. Our cohort of 85 cases included COVID-19 patients who died a few days after infection with SARS-CoV-2, enabling us to catch the virus while it was still replicating. We found that sustentacular cells are the major target cell type in the olfactory mucosa. We failed to find evidence for infection of olfactory sensory neurons, and the parenchyma of the olfactory bulb is spared as well. Thus, SARS-CoV-2 does not appear to be a neurotropic virus. We postulate that transient insufficient support from sustentacular cells triggers transient olfactory dysfunction in COVID-19. Olfactory sensory neurons would become affected without getting infected. ll
Purpose of Review
Despite 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 Findings
TRP 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.
Summary
The 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.
LETTERScofactors and in patient 3 from 5 g gluten to 80 g gluten with cofactors (Table 1). Of note, no patient developed anaphylaxis despite continuous consumption of wheat products during the treatment. After 6 and 9 months of treatment, patient 2 developed urticaria after eating pancake and patient 3 after consuming spaghetti, both followed by mild exercise. No further systemic reactions occurred afterwards.The results of this first study demonstrate that SLIT with gluten increases the reaction threshold of tolerated gluten with / without cofactors. Titrated SPT, specific IgE and BAT seem not to be predictive parameters, hence OCT remains gold standard for threshold determination. These results are in agreement with a Danish study assessing the influence of diet on wheat intake tolerance reporting a diet without total avoidance of gluten products to be associated with developing an increased reaction threshold. 6 However, further studies with a larger population are necessary to confirm our results in this pilot study.
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