Evidence map›Paper›PMID 32983087›Full record

ArticleFrontiers in immunology2020

Complement C5a Induces Pro-inflammatory Microvesicle Shedding in Severely Injured Patients.

Ebru Karasu, Julia Demmelmaier, Stephanie Kellermann, Karlheinz Holzmann, Jörg Köhl, Christoph Q Schmidt, Miriam Kalbitz, Florian Gebhard, Markus S Huber-Lang, Rebecca Halbgebauer

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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  4. Exosome-primed T cell immunity is facilitated by complement activation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026
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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

10 authors at 3 institutions in 2 countries.

Ebru KarasuInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.
Julia DemmelmaierInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.
Stephanie KellermannInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.
Karlheinz HolzmannCenter for Biomedical Research, Genomics-Core Facility, Ulm University, Ulm, Germany.
Jörg KöhlInstitute for Systemic Inflammation Research (ISEF), University of Lübeck, Lübeck, Germany.
Christoph Q SchmidtInstitute of Pharmacology of Natural Products and Clinical Pharmacology, Ulm University, Ulm, Germany.
Miriam KalbitzDepartment of Traumatology, Hand-, Plastic- and Reconstructive Surgery, Center of Surgery, University of Ulm Medical School, Ulm, Germany.
Florian GebhardDepartment of Traumatology, Hand-, Plastic- and Reconstructive Surgery, Center of Surgery, University of Ulm Medical School, Ulm, Germany.
Markus S Huber-LangInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.
Rebecca HalbgebauerInstitute of Clinical and Experimental Trauma Immunology, University Hospital Ulm, Ulm, Germany.
University Hospital Ulm · DEUniversität Ulm · DECincinnati Children's Hospital Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Initially underestimated as platelet dust, extracellular vesicles are continuously gaining interest in the field of inflammation. Various studies addressing inflammatory diseases have shown that microvesicles (MVs) originating from different cell types are systemic transport vehicles carrying distinct cargoes to modulate immune responses. In this study, we focused on the clinical setting of multiple trauma, which is characterized by activation and dysfunction of both, the fluid-phase and the cellular component of innate immunity. Given the sensitivity of neutrophils for the complement anaphylatoxin C5a, we hypothesized that increased C5a production induces alterations in MV shedding of neutrophils resulting in neutrophil dysfunction that fuels posttraumatic inflammation. In a mono-centered prospective clinical study with polytraumatized patients, we found significantly increased granulocyte-derived MVs containing the C5a receptor (C5aR1, CD88) on their surface. This finding was accompanied by a concomitant loss of C5aR1 on granulocytes indicative of an impaired cellular chemotactic and pro-inflammatory neutrophil functions. Furthermore,

Indexed as

Immunity, InnateADP-Ribosylation Factor 6ADP-Ribosylation FactorsAdultCase-Control StudiesCell-Derived MicroparticlesComplement C5aFemaleHumansInflammation MediatorsInjury Severity ScoreInterleukin-6KineticsMaleMiddle AgedMultiple TraumaADP-Ribosylation Factor 6ADP-Ribosylation FactorsARF6 protein, humanC5AR1 protein, humanComplement C5aIL6 protein, humanInflammation MediatorsInterleukin-6MPO protein, humanNADPPeroxidaseReactive Oxygen SpeciesReceptor, Anaphylatoxin C5aanaphylatoxin C5aC5aR1inflammationmicrovesicle sheddingmultiple traumaneutrophilspolymorphonuclear neutrophils (PMNs)

Identifiers

PMID32983087
PMCPMC7492592
OpenAlexW3082195108

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.