Format

Send to

Choose Destination
See comment in PubMed Commons below
Clin Infect Dis. 2014 Aug 15;59(4):e66-71. doi: 10.1093/cid/ciu276. Epub 2014 Apr 24.

Mannose-binding lectin gene, MBL2, polymorphisms are not associated with susceptibility to invasive pneumococcal disease in children.

Author information

  • 1Department of Infectious Diseases Clinical Research Centre, Hvidovre Hospital, University of Copenhagen, Hvidovre Faculty of Health Sciences, University of Copenhagen, Copenhagen.
  • 2Department of Infectious Diseases, Rigshospitalet, Copenhagen University Hospital Department of Microbiological Surveillance and Research, Statens Serum Institut, Copenhagen, Denmark.
  • 3Department of Infectious Diseases Clinical Research Centre, Hvidovre Hospital, University of Copenhagen, Hvidovre.
  • 4Department of Clinical Biochemistry, Immunology and Genetics, Statens Serum Institut, Copenhagen.
  • 5Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus.
  • 6Department of Microbiological Surveillance and Research, Statens Serum Institut, Copenhagen, Denmark.

Abstract

BACKGROUND:

Most children are transiently colonized with Streptococcus pneumoniae, but very few develop invasive pneumococcal disease (IPD). Host genetic variation of innate immunity may predispose to IPD. We investigated the effect of genetic variation in the mannose-binding lectin gene, MBL2, on susceptibility and disease severity of IPD in previously healthy children aged <5 years.

METHODS:

IPD cases were identified through national registries. DNA was obtained from the Danish Neonatal Screening Biobank. Pneumococcal serotypes were determined by Quellung reaction. The associations between MBL2 diplotypes and IPD susceptibility, serotypes, and outcome were investigated using logistic regression analysis.

RESULTS:

We included 372 cases with meningitis, 907 with bacteremia, and 1263 age- and sex-matched controls; 2372 individuals were successfully genotyped and assigned MBL2 diplotypes. The median age in our combined case series was 13 months. Children with defective diplotypes were not at higher risk for meningitis than children with other diplotypes (odds ratio [OR], 0.85; 95% confidence interval [CI], .56-1.28). Similar results were found for bacteremia (OR, 0.89; 95% CI, .68-1.15) as well as for all cases (OR, 0.87; 95% CI, .70-1.09). There was no association with susceptibility to recurrent IPD (n = 12) for children with defective diplotypes compared with cases with a single episode (OR, 0.53; 95% CI, .07-4.13) and with all controls (OR, 0.46; 95% CI, .06-3.56). There was no association between diplotypes and mortality or between diplotypes and pneumococcal serotypes.

CONCLUSIONS:

Defective MBL2 polymorphisms did not predict increased IPD susceptibility in children born in Northern Europe.

© The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

KEYWORDS:

MBL deficiency; MBL2 genotypes; invasive pneumococcal disease; pneumococcal serotypes

[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Write to the Help Desk