Evidence map›Paper›PMID 31883521›Full record

ArticleJournal of neuroinflammation2019

Complement factor H contributes to mortality in humans and mice with bacterial meningitis.

E Soemirien Kasanmoentalib, Mercedes Valls Serón, Joo Yeon Engelen-Lee, Michael W Tanck, Richard B Pouw, Gerard van Mierlo, Diana Wouters, Matthew C Pickering, Arie van der Ende, Taco W Kuijpers and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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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 5 institutions in 2 countries.

E Soemirien KasanmoentalibDepartment of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands.
Mercedes Valls SerónDepartment of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands.
Joo Yeon Engelen-LeeDepartment of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands.
Michael W TanckDepartment of Clinical Epidemiology, Biostatistics and Bioinformatics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Richard B PouwDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Gerard van MierloDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Diana WoutersDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Matthew C PickeringCentre for Inflammatory Disease, Division of Immunology and Inflammation, Department of Medicine, Imperial College London, London, UK.
Arie van der EndeDepartment of Medical Microbiology and The Netherlands Reference Laboratory for Bacterial Meningitis, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Taco W KuijpersDepartment of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Matthijs C BrouwerDepartment of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands.
Diederik van de BeekDepartment of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands. d.vandebeek@amsterdamumc.nl.
Amsterdam University Medical Centers · NLUniversity of Amsterdam · NLAmsterdam Neuroscience · NLImperial College London · GBSanquin · NL

Funding

European Union, EUCLIDS EC-GA no. 279185H2020 European Research Council 281156Wellcome Trust 212252/Z/18/ZZonMw 016.116.358ZonMw 916.13.078 and 917.17.308
6 · The paper itself

Abstract

backgroundThe complement system is a vital component of the inflammatory response occurring during bacterial meningitis. Blocking the complement system was shown to improve the outcome of experimental pneumococcal meningitis. Complement factor H (FH) is a complement regulatory protein inhibiting alternative pathway activation but is also exploited by the pneumococcus to prevent complement activation on its surface conferring serum resistance.

methodsIn a nationwide prospective cohort study of 1009 episodes with community-acquired bacterial meningitis, we analyzed whether genetic variations in CFH influenced FH cerebrospinal fluid levels and/or disease severity. Subsequently, we analyzed the role of FH in our pneumococcal meningitis mouse model using FH knock-out (Cfh

resultsWe found the major allele (G) of single nucleotide polymorphism in CFH (rs6677604) to be associated with low FH cerebrospinal fluid concentration and increased mortality. In patients and mice with bacterial meningitis, FH concentrations were elevated during disease and Cfh

conclusionLow FH levels contribute to mortality in pneumococcal meningitis but adjuvant treatment with FH at a clinically relevant time point is not beneficial.

Indexed as

AdultAgedAnimalsComplement Factor HFemaleHumansMaleMeningitis, BacterialMiceMice, KnockoutMiddle AgedPolymorphism, Single NucleotideComplement Factor HAnimal modelsAnti-inflammatory therapyBacterial meningitisComplement factor HComplement systemPneumococcal meningitis

Identifiers

PMID31883521
PMCPMC6935240
OpenAlexW2998366011

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.