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Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19
The leading cause of mortality from COVID-19 infection is respiratory distress due to an exaggerated host immune response, resulting in hyper-inflammation and ensuing cytokine storms in the lungs. Current drug-based therapies are of limited efficacy, costly, and have potential negative side effects....
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8451450/ https://www.ncbi.nlm.nih.gov/pubmed/34552685 http://dx.doi.org/10.1080/19420889.2021.1965718 |
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author | Aguida, Blanche Pooam, Marootpong Ahmad, Margaret Jourdan, Nathalie |
author_facet | Aguida, Blanche Pooam, Marootpong Ahmad, Margaret Jourdan, Nathalie |
author_sort | Aguida, Blanche |
collection | PubMed |
description | The leading cause of mortality from COVID-19 infection is respiratory distress due to an exaggerated host immune response, resulting in hyper-inflammation and ensuing cytokine storms in the lungs. Current drug-based therapies are of limited efficacy, costly, and have potential negative side effects. By contrast, photobiomodulation therapy, which involves periodic brief exposure to red or infrared light, is a noninvasive, safe, and affordable method that is currently being used to treat a wide range of diseases with underlying inflammatory conditions. Here, we show that exposure to two 10-min, high-intensity periods per day of infrared light causes a marked reduction in the TLR-4 dependent inflammatory response pathway, which has been implicated in the onset of cytokine storms in COVID-19 patients. Infrared light exposure resulted in a significant decline in NFkB and AP1 activity as measured by the reporter gene assay; decreased expression of inflammatory marker genes IL-6, IL-8, TNF-alpha, INF-alpha, and INF-beta as determined by qPCR gene expression assay; and an 80% decline in secreted cytokine IL6 as measured by ELISA assay in cultured human cells. All of these changes occurred after only 48 hours of treatment. We suggest that an underlying cellular mechanism involving modulation of ROS may downregulate the host immune response after Infrared Light exposure, leading to decrease in inflammation. We further discuss technical considerations involving light sources and exposure conditions to put these observations into potential clinical use to treat COVID-19 induced mortality. |
format | Online Article Text |
id | pubmed-8451450 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-84514502021-09-21 Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19 Aguida, Blanche Pooam, Marootpong Ahmad, Margaret Jourdan, Nathalie Commun Integr Biol Short Communication The leading cause of mortality from COVID-19 infection is respiratory distress due to an exaggerated host immune response, resulting in hyper-inflammation and ensuing cytokine storms in the lungs. Current drug-based therapies are of limited efficacy, costly, and have potential negative side effects. By contrast, photobiomodulation therapy, which involves periodic brief exposure to red or infrared light, is a noninvasive, safe, and affordable method that is currently being used to treat a wide range of diseases with underlying inflammatory conditions. Here, we show that exposure to two 10-min, high-intensity periods per day of infrared light causes a marked reduction in the TLR-4 dependent inflammatory response pathway, which has been implicated in the onset of cytokine storms in COVID-19 patients. Infrared light exposure resulted in a significant decline in NFkB and AP1 activity as measured by the reporter gene assay; decreased expression of inflammatory marker genes IL-6, IL-8, TNF-alpha, INF-alpha, and INF-beta as determined by qPCR gene expression assay; and an 80% decline in secreted cytokine IL6 as measured by ELISA assay in cultured human cells. All of these changes occurred after only 48 hours of treatment. We suggest that an underlying cellular mechanism involving modulation of ROS may downregulate the host immune response after Infrared Light exposure, leading to decrease in inflammation. We further discuss technical considerations involving light sources and exposure conditions to put these observations into potential clinical use to treat COVID-19 induced mortality. Taylor & Francis 2021-09-15 /pmc/articles/PMC8451450/ /pubmed/34552685 http://dx.doi.org/10.1080/19420889.2021.1965718 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 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 use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Short Communication Aguida, Blanche Pooam, Marootpong Ahmad, Margaret Jourdan, Nathalie Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19 |
title | Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19 |
title_full | Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19 |
title_fullStr | Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19 |
title_full_unstemmed | Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19 |
title_short | Infrared light therapy relieves TLR-4 dependent hyper-inflammation of the type induced by COVID-19 |
title_sort | infrared light therapy relieves tlr-4 dependent hyper-inflammation of the type induced by covid-19 |
topic | Short Communication |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8451450/ https://www.ncbi.nlm.nih.gov/pubmed/34552685 http://dx.doi.org/10.1080/19420889.2021.1965718 |
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