Evidence map›Paper›PMID 34192268›Full record

ArticleOxford open immunology2020

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, Shayda Maleki-Toyserkani, Felix C Richter and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oxford open immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Patrícia R S RodriguesDivision of Infection and Immunity, School of Medicine, Systems Immunity Research Institute, Cardiff University, Cardiff, UK.
Aljawharah AlrubayyiNuffield Department of Medicine, Viral Immunology Unit, University of Oxford, Oxford, UK.
Ellie PringDivision of Infection and Immunity, School of Medicine, Systems Immunity Research Institute, Cardiff University, Cardiff, UK.
Valentina M T BartDivision of Infection and Immunity, School of Medicine, Systems Immunity Research Institute, Cardiff University, Cardiff, UK.
Ruth JonesDementia Research Institute, Division of Infection and Immunity, School of Medicine, Cardiff University, Cardiff, UK.
Clarissa CoveneyKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.
Fangfang LuSir William Dunn School of Pathology, University of Oxford, Oxford, UK.
Michael TellierSir William Dunn School of Pathology, University of Oxford, Oxford, UK.ORCID 0000-0002-4130-9050
Shayda Maleki-ToyserkaniDivision of Infection and Immunity, School of Medicine, Systems Immunity Research Institute, Cardiff University, Cardiff, UK.
Felix C RichterKennedy Institute of Rheumatology, University of Oxford, Oxford, UK.ORCID 0000-0002-3415-3449
D Oliver ScourfieldDivision of Infection and Immunity, School of Medicine, Systems Immunity Research Institute, Cardiff University, Cardiff, UK.
Ester Gea-MallorquíNuffield Department of Medicine, Viral Immunology Unit, University of Oxford, Oxford, UK.ORCID 0000-0002-6915-074X
Luke C DaviesDivision of Infection and Immunity, School of Medicine, Systems Immunity Research Institute, Cardiff University, Cardiff, UK.ORCID 0000-0001-7767-4060

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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, 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.

Indexed as

COVID-19Innate immunologyMacrophagesMonocytesNeutrophilsNK cells

Identifiers

PMID34192268
PMCPMC7798612

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.