Inflammatory Cytokine: IL-17A Signaling Pathway in Patients Present with COVID-19 and Current Treatment Strategy
Tewodros Shibabaw Department of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, EthiopiaCorrespondence: Tewodros ShibabawDepartment of Biochemistry, School of Medicine, University of Gondar, P.O. Box 196, Gondar, EthiopiaTel +251910162171Email...
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Dove Medical Press
2020
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oai:doaj.org-article:55001c93c91743d5a504a9750685497b2021-12-02T12:59:32ZInflammatory Cytokine: IL-17A Signaling Pathway in Patients Present with COVID-19 and Current Treatment Strategy1178-7031https://doaj.org/article/55001c93c91743d5a504a9750685497b2020-10-01T00:00:00Zhttps://www.dovepress.com/inflammatory-cytokine-il-17a-signaling-pathway-in-patients-present-wit-peer-reviewed-article-JIRhttps://doaj.org/toc/1178-7031Tewodros Shibabaw Department of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, EthiopiaCorrespondence: Tewodros ShibabawDepartment of Biochemistry, School of Medicine, University of Gondar, P.O. Box 196, Gondar, EthiopiaTel +251910162171Email shitewodros@gmail.comAbstract: Coronavirus disease 2019 (COVID-19) is a globally communicable public health disease caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV-2). Eradication of COVID-19 appears practically impossible but, therefore, more effective pharmacotherapy is needed. The deteriorated clinical presentation of patients with COVID-19 is mainly associated with hypercytokinemia due to notoriously elevated pro-inflammatory cytokines such as interleukin (IL)-1B, IL-6, IL-8, IL-17, granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), interferon-γ-inducible protein (IP10), monocyte chemoattractant protein (MCP1), and tumor necrosis factor-α (TNFα), and is usually responsible for cytokine release syndrome. In the cytokine storm, up-regulation of T-helper 17 cell cytokine IL-17A, and maybe also IL-17F, is mostly responsible for the immunopathology of COVID-19 and acute respiratory distress syndrome. Herein, I meticulously review the exuberant polarization mechanism of naïve CD4+ T cells toward Th17 cells in response to SARS-CoV-2 infection and its associated immunopathological sequelae. I also, propose, for clinical benefit, targeting IL-17A signaling and the synergic inflammatory cytokine IL-6 to manage COVID-19 patients, particularly those presenting with cytokine storm syndrome.Keywords: IL-17A, inflammation, immunopathology, COVID-19, cytokine storm, Th17, IL-6, ARDSShibabaw TDove Medical Pressarticleil-17ainflammationimmunopathologycovid-19cytokine stormth17il-6ardsPathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 13, Pp 673-680 (2020) |
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il-17a inflammation immunopathology covid-19 cytokine storm th17 il-6 ards Pathology RB1-214 Therapeutics. Pharmacology RM1-950 |
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il-17a inflammation immunopathology covid-19 cytokine storm th17 il-6 ards Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Shibabaw T Inflammatory Cytokine: IL-17A Signaling Pathway in Patients Present with COVID-19 and Current Treatment Strategy |
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Tewodros Shibabaw Department of Biochemistry, School of Medicine, College of Medicine and Health Sciences, University of Gondar, Gondar, EthiopiaCorrespondence: Tewodros ShibabawDepartment of Biochemistry, School of Medicine, University of Gondar, P.O. Box 196, Gondar, EthiopiaTel +251910162171Email shitewodros@gmail.comAbstract: Coronavirus disease 2019 (COVID-19) is a globally communicable public health disease caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV-2). Eradication of COVID-19 appears practically impossible but, therefore, more effective pharmacotherapy is needed. The deteriorated clinical presentation of patients with COVID-19 is mainly associated with hypercytokinemia due to notoriously elevated pro-inflammatory cytokines such as interleukin (IL)-1B, IL-6, IL-8, IL-17, granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte colony-stimulating factor (G-CSF), interferon-γ-inducible protein (IP10), monocyte chemoattractant protein (MCP1), and tumor necrosis factor-α (TNFα), and is usually responsible for cytokine release syndrome. In the cytokine storm, up-regulation of T-helper 17 cell cytokine IL-17A, and maybe also IL-17F, is mostly responsible for the immunopathology of COVID-19 and acute respiratory distress syndrome. Herein, I meticulously review the exuberant polarization mechanism of naïve CD4+ T cells toward Th17 cells in response to SARS-CoV-2 infection and its associated immunopathological sequelae. I also, propose, for clinical benefit, targeting IL-17A signaling and the synergic inflammatory cytokine IL-6 to manage COVID-19 patients, particularly those presenting with cytokine storm syndrome.Keywords: IL-17A, inflammation, immunopathology, COVID-19, cytokine storm, Th17, IL-6, ARDS |
format |
article |
author |
Shibabaw T |
author_facet |
Shibabaw T |
author_sort |
Shibabaw T |
title |
Inflammatory Cytokine: IL-17A Signaling Pathway in Patients Present with COVID-19 and Current Treatment Strategy |
title_short |
Inflammatory Cytokine: IL-17A Signaling Pathway in Patients Present with COVID-19 and Current Treatment Strategy |
title_full |
Inflammatory Cytokine: IL-17A Signaling Pathway in Patients Present with COVID-19 and Current Treatment Strategy |
title_fullStr |
Inflammatory Cytokine: IL-17A Signaling Pathway in Patients Present with COVID-19 and Current Treatment Strategy |
title_full_unstemmed |
Inflammatory Cytokine: IL-17A Signaling Pathway in Patients Present with COVID-19 and Current Treatment Strategy |
title_sort |
inflammatory cytokine: il-17a signaling pathway in patients present with covid-19 and current treatment strategy |
publisher |
Dove Medical Press |
publishDate |
2020 |
url |
https://doaj.org/article/55001c93c91743d5a504a9750685497b |
work_keys_str_mv |
AT shibabawt inflammatorycytokineil17asignalingpathwayinpatientspresentwithcovid19andcurrenttreatmentstrategy |
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1718393563126956032 |