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Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology

Patrícia R S Rodrigues, Aljawharah Alrubayyi, Ellie Pring, Valentina M T Bart, Ruth Jones, Clarissa Coveney, Fangfang Lu, Michael Tellier Orcid Logo, Shayda Maleki-Toyserkani, Felix C Richter Orcid Logo, D Oliver Scourfield, Ester Gea-Mallorquí Orcid Logo, Luke Davies Orcid Logo

Oxford Open Immunology, Volume: 1, Issue: 1

Swansea University Author: Luke Davies Orcid Logo

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DOI (Published version): 10.1093/oxfimm/iqaa005

Abstract

The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a global health crisis and will likely continue to impact public health for years. As the effectiveness of the innate immune response is crucial to patient outcome...

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Published in: Oxford Open Immunology
ISSN: 2633-6960
Published: Oxford University Press (OUP) 2020
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URI: https://cronfa.swan.ac.uk/Record/cronfa61696
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As the effectiveness of the innate immune response is crucial to patient outcome, huge efforts have been made to understand how dysregulated immune responses may contribute to disease progression. Here we have reviewed current knowledge of cellular innate immune responses to SARS-CoV-2 infection, highlighting areas for further investigation and suggesting potential strategies for intervention. We conclude that in severe COVID-19 initial innate responses, primarily type I interferon, are suppressed or sabotaged which results in an early interleukin (IL)-6, IL-10 and IL-1&#x3B2;-enhanced hyperinflammation. This inflammatory environment is driven by aberrant function of innate immune cells: monocytes, macrophages and natural killer cells dispersing viral pathogen-associated molecular patterns and damage-associated molecular patterns into tissues. This results in primarily neutrophil-driven pathology including fibrosis that causes acute respiratory distress syndrome. Activated leukocytes and neutrophil extracellular traps also promote immunothrombotic clots that embed into the lungs and kidneys of severe COVID-19 patients, are worsened by immobility in the intensive care unit and are perhaps responsible for the high mortality. 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spelling 2022-11-07T14:21:11.2120226 v2 61696 2022-10-31 Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology ff080296775381560053d5e3a6e81745 0000-0001-7767-4060 Luke Davies Luke Davies true false 2022-10-31 BMS The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a global health crisis and will likely continue to impact public health for years. As the effectiveness of the innate immune response is crucial to patient outcome, huge efforts have been made to understand how dysregulated immune responses may contribute to disease progression. Here we have reviewed current knowledge of cellular innate immune responses to SARS-CoV-2 infection, highlighting areas for further investigation and suggesting potential strategies for intervention. We conclude that in severe COVID-19 initial innate responses, primarily type I interferon, are suppressed or sabotaged which results in an early interleukin (IL)-6, IL-10 and IL-1β-enhanced hyperinflammation. This inflammatory environment is driven by aberrant function of innate immune cells: monocytes, macrophages and natural killer cells dispersing viral pathogen-associated molecular patterns and damage-associated molecular patterns into tissues. This results in primarily neutrophil-driven pathology including fibrosis that causes acute respiratory distress syndrome. Activated leukocytes and neutrophil extracellular traps also promote immunothrombotic clots that embed into the lungs and kidneys of severe COVID-19 patients, are worsened by immobility in the intensive care unit and are perhaps responsible for the high mortality. Therefore, treatments that target inflammation and coagulation are promising strategies for reducing mortality in COVID-19. Journal Article Oxford Open Immunology 1 1 Oxford University Press (OUP) 2633-6960 Innate immunology, COVID-19, Neutrophils, Monocytes, NK cells, Macrophages 8 12 2020 2020-12-08 10.1093/oxfimm/iqaa005 COLLEGE NANME Biomedical Sciences COLLEGE CODE BMS Swansea University 2022-11-07T14:21:11.2120226 2022-10-31T12:37:27.2264405 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine Patrícia R S Rodrigues 1 Aljawharah Alrubayyi 2 Ellie Pring 3 Valentina M T Bart 4 Ruth Jones 5 Clarissa Coveney 6 Fangfang Lu 7 Michael Tellier 0000-0002-4130-9050 8 Shayda Maleki-Toyserkani 9 Felix C Richter 0000-0002-3415-3449 10 D Oliver Scourfield 11 Ester Gea-Mallorquí 0000-0002-6915-074x 12 Luke Davies 0000-0001-7767-4060 13 61696__25672__35056fb3ee4c4345aea90fd7c8055ea5.pdf 61696.pdf 2022-11-07T14:20:03.0589485 Output 756270 application/pdf Version of Record true Copyright: The Author(s) 2020. This is an Open Access article distributed under the terms of the Creative Commons Attribution License. true eng http://creativecommons.org/licenses/by/4.0/
title Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology
spellingShingle Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology
Luke Davies
title_short Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology
title_full Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology
title_fullStr Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology
title_full_unstemmed Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology
title_sort Innate immunology in COVID-19—a living review. Part II: dysregulated inflammation drives immunopathology
author_id_str_mv ff080296775381560053d5e3a6e81745
author_id_fullname_str_mv ff080296775381560053d5e3a6e81745_***_Luke Davies
author Luke Davies
author2 Patrícia R S Rodrigues
Aljawharah Alrubayyi
Ellie Pring
Valentina M T Bart
Ruth Jones
Clarissa Coveney
Fangfang Lu
Michael Tellier
Shayda Maleki-Toyserkani
Felix C Richter
D Oliver Scourfield
Ester Gea-Mallorquí
Luke Davies
format Journal article
container_title Oxford Open Immunology
container_volume 1
container_issue 1
publishDate 2020
institution Swansea University
issn 2633-6960
doi_str_mv 10.1093/oxfimm/iqaa005
publisher Oxford University Press (OUP)
college_str Faculty of Medicine, Health and Life Sciences
hierarchytype
hierarchy_top_id facultyofmedicinehealthandlifesciences
hierarchy_top_title Faculty of Medicine, Health and Life Sciences
hierarchy_parent_id facultyofmedicinehealthandlifesciences
hierarchy_parent_title Faculty of Medicine, Health and Life Sciences
department_str Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine
document_store_str 1
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description The current pandemic of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a global health crisis and will likely continue to impact public health for years. As the effectiveness of the innate immune response is crucial to patient outcome, huge efforts have been made to understand how dysregulated immune responses may contribute to disease progression. Here we have reviewed current knowledge of cellular innate immune responses to SARS-CoV-2 infection, highlighting areas for further investigation and suggesting potential strategies for intervention. We conclude that in severe COVID-19 initial innate responses, primarily type I interferon, are suppressed or sabotaged which results in an early interleukin (IL)-6, IL-10 and IL-1β-enhanced hyperinflammation. This inflammatory environment is driven by aberrant function of innate immune cells: monocytes, macrophages and natural killer cells dispersing viral pathogen-associated molecular patterns and damage-associated molecular patterns into tissues. This results in primarily neutrophil-driven pathology including fibrosis that causes acute respiratory distress syndrome. Activated leukocytes and neutrophil extracellular traps also promote immunothrombotic clots that embed into the lungs and kidneys of severe COVID-19 patients, are worsened by immobility in the intensive care unit and are perhaps responsible for the high mortality. Therefore, treatments that target inflammation and coagulation are promising strategies for reducing mortality in COVID-19.
published_date 2020-12-08T04:20:42Z
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