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Acute Systemic Experimental Inflammation Does Not Reduce Human Odor Identification Performance

Olfactory dysfunction is a common symptom of various diseases, but the underlying pathophysiology has not been fully understood. Evidence from both animal and human studies suggests that local inflammation of the olfactory epithelium is linked to olfactory dysfunction. However, whether systemic infl...

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Autores principales: Tognetti, Arnaud, Sarolidou, Georgia, Lasselin, Julie, Lekander, Mats, Olsson, Mats J, Lundström, Johan N
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8015794/
https://www.ncbi.nlm.nih.gov/pubmed/33537776
http://dx.doi.org/10.1093/chemse/bjab004
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author Tognetti, Arnaud
Sarolidou, Georgia
Lasselin, Julie
Lekander, Mats
Olsson, Mats J
Lundström, Johan N
author_facet Tognetti, Arnaud
Sarolidou, Georgia
Lasselin, Julie
Lekander, Mats
Olsson, Mats J
Lundström, Johan N
author_sort Tognetti, Arnaud
collection PubMed
description Olfactory dysfunction is a common symptom of various diseases, but the underlying pathophysiology has not been fully understood. Evidence from both animal and human studies suggests that local inflammation of the olfactory epithelium is linked to olfactory dysfunction. However, whether systemic inflammation causes olfactory dysfunction is yet to be determined. In the present behavioral study, we set out to test whether acute systemic inflammation impairs olfactory identification performance by inducing a transient and controlled state of systemic inflammation using an experimental endotoxemia model. We treated young healthy participants (N = 20) with a relatively high dose (2.0 ng/kg) of lipopolysaccharide (LPS) and a placebo treatment in a double-blind within-subject design, and assessed participants’ ability to identify odors using the MONEX-40, a reliable method for experimental assessment of odor identification ability in healthy and young individuals. Our results show that olfactory identification performance was not affected by the acute systemic inflammation triggered by the injection of LPS. Moreover, odor identification performance following the LPS injection was not associated with levels of circulating proinflammatory cytokines (interleukin-6, interleukin-8, and tumor necrosis factor-α). Because experimental LPS-induced systemic inflammation does not affect olfactory identification performance, our findings suggest that chronic, rather than transient, systemic inflammation is a more likely mechanism to explore in order to explain the olfactory deficits observed in inflammatory diseases.
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spelling pubmed-80157942021-04-07 Acute Systemic Experimental Inflammation Does Not Reduce Human Odor Identification Performance Tognetti, Arnaud Sarolidou, Georgia Lasselin, Julie Lekander, Mats Olsson, Mats J Lundström, Johan N Chem Senses Special Issue: Clinical Science in the Chemical Senses Olfactory dysfunction is a common symptom of various diseases, but the underlying pathophysiology has not been fully understood. Evidence from both animal and human studies suggests that local inflammation of the olfactory epithelium is linked to olfactory dysfunction. However, whether systemic inflammation causes olfactory dysfunction is yet to be determined. In the present behavioral study, we set out to test whether acute systemic inflammation impairs olfactory identification performance by inducing a transient and controlled state of systemic inflammation using an experimental endotoxemia model. We treated young healthy participants (N = 20) with a relatively high dose (2.0 ng/kg) of lipopolysaccharide (LPS) and a placebo treatment in a double-blind within-subject design, and assessed participants’ ability to identify odors using the MONEX-40, a reliable method for experimental assessment of odor identification ability in healthy and young individuals. Our results show that olfactory identification performance was not affected by the acute systemic inflammation triggered by the injection of LPS. Moreover, odor identification performance following the LPS injection was not associated with levels of circulating proinflammatory cytokines (interleukin-6, interleukin-8, and tumor necrosis factor-α). Because experimental LPS-induced systemic inflammation does not affect olfactory identification performance, our findings suggest that chronic, rather than transient, systemic inflammation is a more likely mechanism to explore in order to explain the olfactory deficits observed in inflammatory diseases. Oxford University Press 2021-02-04 /pmc/articles/PMC8015794/ /pubmed/33537776 http://dx.doi.org/10.1093/chemse/bjab004 Text en © The Author(s) 2021. Published by Oxford University Press. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Special Issue: Clinical Science in the Chemical Senses
Tognetti, Arnaud
Sarolidou, Georgia
Lasselin, Julie
Lekander, Mats
Olsson, Mats J
Lundström, Johan N
Acute Systemic Experimental Inflammation Does Not Reduce Human Odor Identification Performance
title Acute Systemic Experimental Inflammation Does Not Reduce Human Odor Identification Performance
title_full Acute Systemic Experimental Inflammation Does Not Reduce Human Odor Identification Performance
title_fullStr Acute Systemic Experimental Inflammation Does Not Reduce Human Odor Identification Performance
title_full_unstemmed Acute Systemic Experimental Inflammation Does Not Reduce Human Odor Identification Performance
title_short Acute Systemic Experimental Inflammation Does Not Reduce Human Odor Identification Performance
title_sort acute systemic experimental inflammation does not reduce human odor identification performance
topic Special Issue: Clinical Science in the Chemical Senses
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8015794/
https://www.ncbi.nlm.nih.gov/pubmed/33537776
http://dx.doi.org/10.1093/chemse/bjab004
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