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Proinflammatory Cytokines in the Olfactory Mucosa Result in COVID-19 Induced Anosmia
Author(s) -
Abolfazl Torabi,
Esmaeil Mohammadbagheri,
Nader Akbari Dilmaghani,
AmirHossein Bayat,
Mobina Fathi,
Kimia Vakili,
Rafieh Alizadeh,
Omidvar Rezaeimirghaed,
Mohammadreza Hajiesmaeili,
Mahtab Ramezani,
Leila Simani,
Abbas Aliaghaei
Publication year - 2020
Publication title -
acs chemical neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.158
H-Index - 69
ISSN - 1948-7193
DOI - 10.1021/acschemneuro.0c00249
Subject(s) - anosmia , proinflammatory cytokine , olfactory epithelium , olfactory mucosa , olfaction , epithelium , cytokine , olfactory system , tumor necrosis factor alpha , respiratory epithelium , medicine , inflammation , immunology , pathology , covid-19 , biology , disease , neuroscience , infectious disease (medical specialty) , psychiatry
Studies have found increased rates of dysosmia in patients with Novel Coronavirus disease 2019 (COVID-19). However, the mechanism that causes olfactory loss is unknown. The primary objective of this study was to explore local proinflammatory cytokine levels in the olfactory epithelium in patients with COVID-19. Biopsies of the olfactory epithelium were taken from patients with confirmed COVID-19 as well as uninfected controls. Levels of tumor necrosis factor α (TNF-α) and interleukin-1-beta (IL-1β) were assessed using ELISA and compared between groups. Average TNF-α levels were significantly increased in the olfactory epithelium of the COVID-19 group compared to the control group ( P < 0.05). However, no differences in IL-1β were seen between groups. Elevated levels of the proinflammatory cytokine TNF-α were seen in the olfactory epithelium in patients with COVID-19. This suggests that direct inflammation of the olfactory epithelium could play a role in the acute olfactory loss described in many patients with COVID-19.

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