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


Journal

Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974

Informations de publication

Date de publication:
28 Dec 2019
Historique:
received: 02 09 2019
accepted: 16 12 2019
entrez: 30 12 2019
pubmed: 31 12 2019
medline: 15 7 2020
Statut: epublish

Résumé

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

Sections du résumé

BACKGROUND BACKGROUND
The 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.
METHODS METHODS
In 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
RESULTS RESULTS
We 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
CONCLUSION CONCLUSIONS
Low FH levels contribute to mortality in pneumococcal meningitis but adjuvant treatment with FH at a clinically relevant time point is not beneficial.

Identifiants

pubmed: 31883521
doi: 10.1186/s12974-019-1675-1
pii: 10.1186/s12974-019-1675-1
pmc: PMC6935240
doi:

Substances chimiques

Complement Factor H 80295-65-4

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

279

Subventions

Organisme : European Union, EUCLIDS
ID : EC-GA no. 279185
Organisme : ZonMw
ID : 016.116.358
Pays : Netherlands
Organisme : ZonMw
ID : 916.13.078 and 917.17.308
Pays : Netherlands
Organisme : Wellcome Trust
ID : 212252/Z/18/Z
Pays : United Kingdom
Organisme : H2020 European Research Council
ID : 281156

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Auteurs

E Soemirien Kasanmoentalib (ES)

Department of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands.

Mercedes Valls Serón (M)

Department of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands.

Joo Yeon Engelen-Lee (JY)

Department of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands.

Michael W Tanck (MW)

Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.

Richard B Pouw (RB)

Department of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Department of Pediatric Hematology, Immunology and Infectious Diseases, Emma Children's Hospital, Amsterdam UMC, Amsterdam, the Netherlands.

Gerard van Mierlo (G)

Department of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.

Diana Wouters (D)

Department of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.

Matthew C Pickering (MC)

Centre for Inflammatory Disease, Division of Immunology and Inflammation, Department of Medicine, Imperial College London, London, UK.

Arie van der Ende (A)

Department of Medical Microbiology and The Netherlands Reference Laboratory for Bacterial Meningitis, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.

Taco W Kuijpers (TW)

Department of Immunopathology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Department of Pediatric Hematology, Immunology and Infectious Diseases, Emma Children's Hospital, Amsterdam UMC, Amsterdam, the Netherlands.
Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.

Matthijs C Brouwer (MC)

Department of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands.

Diederik van de Beek (D)

Department of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, the Netherlands. d.vandebeek@amsterdamumc.nl.

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Classifications MeSH