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The nasal epithelium expressing enriched angiotensin-converting enzyme II (ACE2), the key cell entry receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), could serve as the first barrier to protect the airway from viral infection. Recent studies have demonstrated that higher viral loads were detected in the nasal cavity than the pharynx in coronavirus disease 2019 (COVID-19) patients, and otolaryngologists should carefully consider infection prevention in clinical practice for the treatment of nasal conditions. Moreover, several studies have indicated that anosmia is one of the clinical characteristics of COVID-19, but the precise prevalence and mechanism remain unclear. Thus far, comorbidity of allergic rhinitis and chronic rhinosinusitis do not seem to be a major risk factor for severe COVID-19. However, we should develop strategies in clinical practice for treatment of nasal diseases during the pandemic. In this article, we reviewed current evidence of the relationship between COVID-19 and nasal conditions, such as COVID-19-related olfactory dysfunction, allergic rhinitis, and chronic rhinosinusitis., (Copyright© 2021, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Low-dose and long-term administration of 14-membered macrolide antibiotics is well-known to be effective in the treatment of chronic airway diseases. Although there is much evidence that the anti-inflammatory action, but not the anti-microbial action of macrolides, is responsible for the clinical efficacy of these agents on chronic airway inflammatory diseases, the precise therapeutic mechanisms are not well-understood. Since thioredoxin (TRX) has now attracted attention as an endogenous peptide with immunomodulatory effects, the present study was undertaken to examine whether macrolide antibiotics could favorably modulate the clinical status of such diseases via the production of TRX from nasal epithelial cells in vitro. Nasal epithelial cells (5×10(5) cells/ml) obtained from five patients were stimulated with 50 μM H2O2 in the presence of different concentrations of macrolide antibiotics for 24 h. TRX levels in culture supernatants were examined by enzyme-linked immunosorbent assay. We also examined the influence of macrolide antibiotics on TRX mRNA expression and mRNA translation by RT-PCR and a wheat germ cell-free protein synthesis technique, respectively. The addition of clarithromycin (CAM) to cell cultures caused an increase in the ability of cells to produce TRX in response to H2O2 stimulation, and the minimum concentration that caused a significant increase was 0.5 μg/ml. On the other hand, josamycin, a 16-membered macrolide antibiotic, did not increase TRX production induced by H2O2 stimulation. Although the treatment of cells with CAM inhibits TRX mRNA transcription, the agent might increase translation of mRNA to produce specific proteins. The ability of CAM to increase TRX production may account, at least in part, for the clinical efficacy of this agent on chronic airway inflammatory diseases, including chronic rhinosinositis.