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Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions

Host innate immune response follows severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and it is the driver of the acute respiratory distress syndrome (ARDS) amongst other inflammatory end-organ morbidities. Such life-threatening coronavirus disease 2019 (COVID-19) is heralded b...

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Autores principales: Abdelmoaty, Mai M., Yeapuri, Pravin, Machhi, Jatin, Olson, Katherine E., Shahjin, Farah, Kumar, Vikas, Zhou, You, Liang, Jingjing, Pandey, Kabita, Acharya, Arpan, Byrareddy, Siddappa N., Mosley, R. Lee, Gendelman, Howard E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8521106/
https://www.ncbi.nlm.nih.gov/pubmed/34671355
http://dx.doi.org/10.3389/fimmu.2021.741502
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author Abdelmoaty, Mai M.
Yeapuri, Pravin
Machhi, Jatin
Olson, Katherine E.
Shahjin, Farah
Kumar, Vikas
Zhou, You
Liang, Jingjing
Pandey, Kabita
Acharya, Arpan
Byrareddy, Siddappa N.
Mosley, R. Lee
Gendelman, Howard E.
author_facet Abdelmoaty, Mai M.
Yeapuri, Pravin
Machhi, Jatin
Olson, Katherine E.
Shahjin, Farah
Kumar, Vikas
Zhou, You
Liang, Jingjing
Pandey, Kabita
Acharya, Arpan
Byrareddy, Siddappa N.
Mosley, R. Lee
Gendelman, Howard E.
author_sort Abdelmoaty, Mai M.
collection PubMed
description Host innate immune response follows severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and it is the driver of the acute respiratory distress syndrome (ARDS) amongst other inflammatory end-organ morbidities. Such life-threatening coronavirus disease 2019 (COVID-19) is heralded by virus-induced activation of mononuclear phagocytes (MPs; monocytes, macrophages, and dendritic cells). MPs play substantial roles in aberrant immune secretory activities affecting profound systemic inflammation and end-organ malfunctions. All follow the presence of persistent viral components and virions without evidence of viral replication. To elucidate SARS-CoV-2-MP interactions we investigated transcriptomic and proteomic profiles of human monocyte-derived macrophages. While expression of the SARS-CoV-2 receptor, the angiotensin-converting enzyme 2, paralleled monocyte-macrophage differentiation, it failed to affect productive viral infection. In contrast, simple macrophage viral exposure led to robust pro-inflammatory cytokine and chemokine expression but attenuated type I interferon (IFN) activity. Both paralleled dysregulation of innate immune signaling pathways, specifically those linked to IFN. We conclude that the SARS-CoV-2-infected host mounts a robust innate immune response characterized by a pro-inflammatory storm heralding end-organ tissue damage.
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spelling pubmed-85211062021-10-19 Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions Abdelmoaty, Mai M. Yeapuri, Pravin Machhi, Jatin Olson, Katherine E. Shahjin, Farah Kumar, Vikas Zhou, You Liang, Jingjing Pandey, Kabita Acharya, Arpan Byrareddy, Siddappa N. Mosley, R. Lee Gendelman, Howard E. Front Immunol Immunology Host innate immune response follows severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, and it is the driver of the acute respiratory distress syndrome (ARDS) amongst other inflammatory end-organ morbidities. Such life-threatening coronavirus disease 2019 (COVID-19) is heralded by virus-induced activation of mononuclear phagocytes (MPs; monocytes, macrophages, and dendritic cells). MPs play substantial roles in aberrant immune secretory activities affecting profound systemic inflammation and end-organ malfunctions. All follow the presence of persistent viral components and virions without evidence of viral replication. To elucidate SARS-CoV-2-MP interactions we investigated transcriptomic and proteomic profiles of human monocyte-derived macrophages. While expression of the SARS-CoV-2 receptor, the angiotensin-converting enzyme 2, paralleled monocyte-macrophage differentiation, it failed to affect productive viral infection. In contrast, simple macrophage viral exposure led to robust pro-inflammatory cytokine and chemokine expression but attenuated type I interferon (IFN) activity. Both paralleled dysregulation of innate immune signaling pathways, specifically those linked to IFN. We conclude that the SARS-CoV-2-infected host mounts a robust innate immune response characterized by a pro-inflammatory storm heralding end-organ tissue damage. Frontiers Media S.A. 2021-10-04 /pmc/articles/PMC8521106/ /pubmed/34671355 http://dx.doi.org/10.3389/fimmu.2021.741502 Text en Copyright © 2021 Abdelmoaty, Yeapuri, Machhi, Olson, Shahjin, Kumar, Zhou, Liang, Pandey, Acharya, Byrareddy, Mosley and Gendelman https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Abdelmoaty, Mai M.
Yeapuri, Pravin
Machhi, Jatin
Olson, Katherine E.
Shahjin, Farah
Kumar, Vikas
Zhou, You
Liang, Jingjing
Pandey, Kabita
Acharya, Arpan
Byrareddy, Siddappa N.
Mosley, R. Lee
Gendelman, Howard E.
Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions
title Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions
title_full Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions
title_fullStr Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions
title_full_unstemmed Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions
title_short Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions
title_sort defining the innate immune responses for sars-cov-2-human macrophage interactions
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8521106/
https://www.ncbi.nlm.nih.gov/pubmed/34671355
http://dx.doi.org/10.3389/fimmu.2021.741502
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