Evidence map›Paper›PMID 35774516›Full record

ArticleHeliyon2022

Immunometabolic analysis shows a distinct cyto-metabotype in Covid-19 compared to sepsis from other causes.

Francesca M Trovato, Salma Mujib, Ellen Jerome, Anna Cavazza, Phillip Morgan, John Smith, Maria Theresa Depante, Kevin O'Reilly, James Luxton, Tracey Mare and 2 more

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Francesca M TrovatoInstitute of Liver Studies, King's College Hospital, London, United Kingdom.
Salma MujibInstitute of Liver Studies, King's College Hospital, London, United Kingdom.
Ellen JeromeInstitute of Liver Studies, King's College Hospital, London, United Kingdom.
Anna CavazzaInstitute of Liver Studies, King's College Hospital, London, United Kingdom.
Phillip MorganInstitute of Liver Studies, King's College Hospital, London, United Kingdom.
John SmithAnaesthetics, Critical Care, Emergency and Trauma Research Delivery Unit, Kings College Hospital, London, United Kingdom.
Maria Theresa DepanteAnaesthetics, Critical Care, Emergency and Trauma Research Delivery Unit, Kings College Hospital, London, United Kingdom.
Kevin O'ReillyAnaesthetics, Critical Care, Emergency and Trauma Research Delivery Unit, Kings College Hospital, London, United Kingdom.
James LuxtonContract R&D Department (Viapath), Kings College Hospital, London, United Kingdom.
Tracey MareContract R&D Department (Viapath), Kings College Hospital, London, United Kingdom.
Salvatore NapoliInstitute of Liver Studies, King's College Hospital, London, United Kingdom.
Mark Jw McPhailInstitute of Liver Studies, King's College Hospital, London, United Kingdom.
King's College Hospital · GBKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: In Covid-19, profound systemic inflammatory responses are accompanied by both metabolic risk factors for severity and, separately, metabolic mechanisms have been shown to underly disease progression. It is unknown whether this reflects similar situations in sepsis or is a unique characteristic of Covid-19. Aims: Define the immunometabolic signature of Covid-19. Methods: 65 patients with Covid-19,19 patients with sepsis and 14 healthy controls were recruited and sampled for plasma, serum and peripheral blood mononuclear cells (PBMCs) through 10 days of critical illness. Metabotyping was performed using the Biocrates p180 kit and multiplex cytokine profiling undertaken. PBMCs underwent phenotyping by flow cytometry. Immune and metabolic readouts were integrated and underwent pathway analysis. Results: Phopsphatidylcholines (PC) are reduced in Covid-19 but greater than in sepsis. Compared to controls, tryptophan is reduced in Covid-19 and inversely correlated with the severity of the disease and IFN-ɣ concentrations, conversely the kyneurine and kyneurine/tryptophan ratio increased in the most severe cases. These metabolic changes were consistent through 2 pandemic waves in our centre. PD-L1 expression in CD8+ T cells, Tregs and CD14+ monocytes was increased in Covid-19 compared to controls. Conclusions: In our cohort, Covid-19 is associated with monocytopenia, increased CD14+ and Treg PD-L1 expression correlating with IFN-ɣ plasma concentration and disease severity (SOFA score). The latter is also associated with metabolic derangements of Tryptophan, LPC 16:0 and PCs. Lipid metabolism, in particular phosphatidylcholines and lysophosphatidylcolines, seems strictly linked to immune response in Covid-19. Our results support the hypothesis that IFN-ɣ -PD-L1 axis might be involved in the cytokine release syndrome typical of severe Covid-19 and the phenomenon persisted through multiple pandemic waves despite use of immunomodulation.

Indexed as

Covid-19Immune checkpointImmunometabolismPhosphatidylcholineTryptophan

Identifiers

PMID35774516
PMCPMC9225950
OpenAlexW4283377589

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.