Evidence map›Paper›PMID 33609650›Full record

ReviewMicrobial pathogenesis2021

The pro-inflammatory cytokines in COVID-19 pathogenesis: What goes wrong?

Dounia Darif, Ikram Hammi, Ayyoub Kihel, Imane El Idrissi Saik, Fadila Guessous, Khadija Akarid

Open access · greenAbstract readReview
In one paragraph

Review in Microbial pathogenesis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 7 pooled it
18.8field-weighted citation impact, top 1% of its field
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

194 citing papers in PubMed, 7 syntheses or guidelines pooled it, 335 citations in OpenAlex.

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  4. Endometriosis and COVID-19: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2022
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  14. Zinc: a metallic shield against cardiac inflammation.Metallomics : integrated biometal science · 2026
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  17. Potential relationships between circulating gene expression ofJournal of Zhejiang University. Science. B · 2025
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134 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 2 countries.

Dounia DarifMolecular Genetics and Immunophysiopathology Research Team, Health and Environment Laboratory, Aïn Chock Faculty of Sciences, Hassan II University of Casablanca (UH2C), Morocco.
Ikram HammiMolecular Genetics and Immunophysiopathology Research Team, Health and Environment Laboratory, Aïn Chock Faculty of Sciences, Hassan II University of Casablanca (UH2C), Morocco.
Ayyoub KihelMolecular Genetics and Immunophysiopathology Research Team, Health and Environment Laboratory, Aïn Chock Faculty of Sciences, Hassan II University of Casablanca (UH2C), Morocco.
Imane El Idrissi SaikImmunopathology of Infectious and Systemic Diseases, Laboratory of Cellular and Molecular Pathology, Faculty of Medicine and Pharmacy, UH2C, Morocco.
Fadila GuessousDepartment of Biological Sciences, Faculty of Medicine, Mohammed VI University of Health Sciences, Casablanca, Morocco; Department of Microbiology, Immunology and Cancer Biology, School of Medicine, University of Virginia, Charlottesville, VA, USA.
Khadija AkaridMolecular Genetics and Immunophysiopathology Research Team, Health and Environment Laboratory, Aïn Chock Faculty of Sciences, Hassan II University of Casablanca (UH2C), Morocco. Electronic address: KHADIJA.AKARID@univh2C.ma.
University of Hassan II Casablanca · MAUniversité Mohammed VI des Sciences et de la Santé · MA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The outbreak of coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, has emerged in China in December 2019 and rapidly spread to more than 196 countries worldwide. The physiopathology of human SARS-CoV-2 has not been completely understood, but its pathogenesis has been linked to a disproportionate response of the immune system. Just as described for SARS and MERS, an uncontrolled systemic inflammatory response, known as cytokine release syndrome (CRS) was observed in severe COVID-19 patients. It results from the release by immune and non-immune effector cells of substantial amounts of pro-inflammatory cytokines and appears to contribute to SARS-CoV-2 pulmonary inflammation and extensive lung damage. In addition, hyper-coagulation and thrombosis resulted from the important release of pro-inflammatory cytokines contribute to the lethality of subjects severely infected with SARS-CoV-2. It is therefore essential to have a deep understanding of the various cytokines involved in this exacerbated immune response, and that could be targeted by potential immunological treatments. The aim of this review was to gather the current knowledge about the role of pro-inflammatory cytokines, namely IL-1β, IL-6, IL-8, IL-17 and TNFα in SARS-CoV-2 CRS, the probable causes and clinical outcomes of this phenomenon in severe cases of COVID-19.

Indexed as

COVID-19Cytokine Release SyndromeCytokinesHumansMacrophage ActivationSARS-CoV-2ThrombosisCytokinesCOVID-19CytokinesInflammationSARS-CoV-2

Identifiers

PMID33609650
PMCPMC7889464
OpenAlexW3130206057

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.