Journal
OPEN FORUM INFECTIOUS DISEASES
Volume 2, Issue 4, Pages -Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/ofid/ofv127
Keywords
invasive meningococcal disease; MBL deficiency; MBL2 genotypes
Categories
Funding
- Lundbeck Foundation
- Novo Nordisk Foundation
- King Christian the 10th Foundation
- Jacob Madsen's Foundation
- TrygVesta, Ebba Celinder's Foundation
- Danish Medical Association Foundation
- Foundation for Advancement of Medical Science
- Augustinus Foundation
- Peder Laurits Pedersen's Foundation
- A.P. Moller Foundation for the Advancement of Medical Science
- Danish Medical Research Council
- Preben and Anna Simonsen's Foundation
- Ferdinand and Ellen Hindsgaul's Foundation
- Hartmann's Foundation
- Dagmar Marshalls Fond
- University of Copenhagen
- Program for Clinical Research Infrastructure by Lundbeck Foundation
- Lundbeck Foundation [R155-2014-2647] Funding Source: researchfish
- Novo Nordisk Fonden [NNF14SA0015794] Funding Source: researchfish
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Background. Neisseria meningitidis is the cause of meningococcal bacteremia and meningitis, and nasopharyngeal colonization with this pathogen is common. The incidence of invasive disease is highest in infants, whereas adolescents more often are carriers. Altered regulation or dysfunction of the innate immune system may predispose to invasive meningococcal disease (IMD). In this study, we investigated the effect of genetic variation in the mannose-binding lectin gene, MBL2, and its promoter on susceptibility to IMD and IMD-associated mortality among children. Methods. Children (<5 years) diagnosed during 1982-2007 with IMD and controls were identified through Danish national registries. DNA was obtained from the Danish Neonatal Screening Biobank. The associations between MBL2 diplotypes and IMD susceptibility and 30-and 90-day mortality were investigated using logistic regression analysis. Results. We included 1351 children: 406 withmeningitis, 272 with bacteremia, and 673 age-and sex-matched controls. Of the children studied, 1292 (96%) were successfully genotyped and assigned MBL2 diplotypes. The median age in IMD cases was 19.1 months (interquartile range [ IQR], 8.8-32.2 months). Children with defective MBL2 diplotypes were not at higher risk for meningococcal meningitis than children with intermediate and normal diplotypes (odds ratio [ OR] = 0.69; 95% confidence interval [ CI],.47-1.02). Similar results were found for children with bacteremia and defective diplotypes (OR = 0.84; 95% CI,.53-1.32) as well as for all cases (OR = 0.75; 95% CI,.56-1.01). There was no association between MBL2 diplotypes and mortality. Conclusions. Defective MBL2 diplotypes did not predict either an increased IMD susceptibility or mortality in a Danish population of children.
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