Evidence map›Paper›PMID 32794348›Full record

Trial reportJournal of leukocyte biology2021

Mismatch between circulating cytokines and spontaneous cytokine production by leukocytes in hyperinflammatory COVID-19.

Robin Kahn, Tobias Schmidt, Karan Golestani, Anki Mossberg, Birgitta Gullstrand, Anders A Bengtsson, Fredrik Kahn

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Journal of leukocyte biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Clinical and Laboratory Approach to Diagnose COVID-19 Using Machine Learning.Interdisciplinary sciences, computational life sciences · 2022
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Endothelial cell, myeloid, and adaptive immune responses in SARS-CoV-2 infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
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

7 authors at 2 institutions in 1 country.

Robin KahnDepartment of Clinical Sciences Lund, Section of Pediatrics, Lund University, Lund, Sweden.
Tobias SchmidtDepartment of Clinical Sciences Lund, Section of Pediatrics, Lund University, Lund, Sweden.
Karan GolestaniSkåne University Hospital, Lund and Malmö, Sweden.
Anki MossbergDepartment of Clinical Sciences Lund, Section of Pediatrics, Lund University, Lund, Sweden.
Birgitta GullstrandDepartment of Clinical Sciences Lund, Rheumatology Lund University, Lund, Sweden.
Anders A BengtssonDepartment of Clinical Sciences Lund, Rheumatology Lund University, Lund, Sweden.
Fredrik KahnSkåne University Hospital, Lund and Malmö, Sweden.
Lund University · SESkåne University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The disease COVID-19 has developed into a worldwide pandemic. Hyperinflammation and high levels of several cytokines, for example, IL-6, are observed in severe COVID-19 cases. However, little is known about the cellular origin of these cytokines. Here, we investigated whether circulating leukocytes from patients with COVID-19 had spontaneous cytokine production. Patients with hyperinflammatory COVID-19 (n = 6) and sepsis (n = 3) were included at Skåne University Hospital, Sweden. Healthy controls were also recruited (n = 5). Cytokines were measured in COVID-19 and sepsis patients using an Immulite immunoassay system. PBMCs were cultured with brefeldin A to allow cytokine accumulation. In parallel, LPS was used as an activator. Cells were analyzed for cytokines and surface markers by flow cytometry. High levels of IL-6 and measurable levels of IL-8 and TNF, but not IL-1β, were observed in COVID-19 patients. Monocytes from COVID-19 patients had spontaneous production of IL-1β and IL-8 (P = 0.0043), but not of TNF and IL-6, compared to controls. No spontaneous cytokine production was seen in lymphocytes from either patients or controls. Activation with LPS resulted in massive cytokine production by monocytes from COVID-19 patients and healthy controls, but not from sepsis patients. Finally, monocytes from COVID-19 patients produced more IL-1β than from healthy controls (P = 0.0087) when activated. In conclusion, monocytes contribute partly to the ongoing hyperinflammation by production of IL-1β and IL-8. Additionally, they are responsive to further activation. This data supports the notion of IL-1β blockade in treatment of COVID-19. However, the source of the high levels of IL-6 remains to be determined.

Indexed as

AgedAged, 80 and overCOVID-19CytokinesFemaleHumansMaleMiddle AgedMonocytesSARS-CoV-2Cytokinescytokine storm, monocytes

Identifiers

PMID32794348
PMCPMC7436862
OpenAlexW3049659113

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.