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Fluoxetine as an anti-inflammatory therapy in SARS-CoV-2 infection.
- Source :
-
Biomedicine & Pharmacotherapy . Jun2021, Vol. 138, pN.PAG-N.PAG. 1p. - Publication Year :
- 2021
-
Abstract
- Hyperinflammatory response caused by infections such as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) increases organ failure, intensive care unit admission, and mortality. Cytokine storm in patients with Coronavirus Disease 2019 (COVID-19) drives this pattern of poor clinical outcomes and is dependent upon the activity of the transcription factor complex nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) and its downstream target gene interleukin 6 (IL6) which interacts with IL6 receptor (IL6R) and the IL6 signal transduction protein (IL6ST or gp130) to regulate intracellular inflammatory pathways. In this study, we compare transcriptomic signatures from a variety of drug-treated or genetically suppressed (i.e. knockdown) cell lines in order to identify a mechanism by which antidepressants such as fluoxetine demonstrate non-serotonergic, anti-inflammatory effects. Our results demonstrate a critical role for IL6ST and NF-kappaB Subunit 1 (NFKB1) in fluoxetine's ability to act as a potential therapy for hyperinflammatory states such as asthma, sepsis, and COVID-19. [Display omitted] • Fluoxetine treatment elicits genetic changes which parallel those caused by IL6ST or NFKB1 knockdown. • Fluoxetine's anti-inflammatory mechanism of action may depend upon NF-kappaB/IL6ST signaling. • The anti-inflammatory effects of fluoxetine are likely independent of its monoaminergic mechanism. • The anti-inflammatory effects of fluoxetine may prevent cytokine storm associated with COVID-19. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 07533322
- Volume :
- 138
- Database :
- Academic Search Index
- Journal :
- Biomedicine & Pharmacotherapy
- Publication Type :
- Academic Journal
- Accession number :
- 149839760
- Full Text :
- https://doi.org/10.1016/j.biopha.2021.111437