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Deficient mannose-binding lectin-mediated complement activation despite mannose-binding lectin-sufficient genotypes

Bjorn L Herpers1, Ed P F Yzerman, Ben A W de Jong

  • 1Department of Medical Microbiology and Immunology, St Antonius Hospital, Nieuwegein, The Netherlands. b.herpers@antonius.net

Human Immunology
|December 17, 2008
PubMed

Insights

Mannose-binding lectin (MBL) deficiency did not increase Legionella infection risk. However, Legionella patients showed reduced MBL complement activation, suggesting this deficiency is a result, not a cause, of infection.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Genetics

Background:

  • Mannose-binding lectin (MBL) deficiency is linked to infection susceptibility but may protect against pathogens using MBL for entry.
  • Legionella pneumophila is an intracellular pathogen, making the role of MBL in Legionnaires' disease complex.

Purpose of the Study:

  • To investigate the association between MBL genotype, MBL activity, and Legionnaires' disease during a large outbreak.
  • To determine if MBL deficiency is a risk factor or a consequence of Legionella pneumophila infection.

Main Methods:

  • Genotyping for MBL2 polymorphisms in 141 patients, 65 exposed staff, and 670 controls.
  • Assessing MBL-mediated complement activation in acute and convalescent phases.
  • Comparing genotypic MBL deficiency prevalence and functional MBL activity between groups.

Main Results:

  • Genotypic MBL deficiency was equally common in patients and controls.
  • Deficient MBL-mediated complement activation was more frequent in patients, even those with MBL-sufficient genotypes.
  • Functional MBL activity often normalized during convalescence in patients with initially sufficient genotypes.

Conclusions:

  • Genotypic MBL deficiency is not a risk factor for Legionnaires' disease.
  • Legionellosis is associated with impaired MBL-mediated complement activation.
  • The observed functional MBL deficiency appears to be an effect of the infection, not a predisposing factor.

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