Mannose-binding lectin genotypes: lack of association with susceptibility to thoracic empyema

To investigate this further we compared the frequencies of the six functional MBL polymorphisms in 170 European individuals with thoracic empyema and 225 healthy control individuals.No overall association was observed between MBL genotypic deficiency and susceptibility to thoracic empyema (2 × 2 Chi square = 0.02, P = 0.87). Furthermore, no association was seen between MBL deficiency and susceptibility to the Gram-positive or pneumococcal empyema subgroups. MBL genotypic deficiency did not associate with progression to death or requirement for surgery.Our results suggest that MBL genotypic deficiency does not associate with susceptibility to thoracic empyema in humans.Mannose-binding lectin (MBL) is a serum lectin which binds repeating sugar arrays on the surface of a wide range of micro-organisms, including Gram-positive bacteria [1]. MBL appears to play an important role in innate immunity by promoting opsonophagocytosis. This occurs primarily through the activation of complement independently of antibody after binding MBL-associated serine proteases (MASPs) 1 and 2. Significant inter-individual variation in baseline serum MBL levels and function occurs as a result of six well-described genetic polymorphisms in the MBL2 gene: three structural polymorphisms and three promoter polymorphisms [2]. The structural polymorphisms consist of non-synonymous polymorphisms in codons 52, 54, or 57, where the mutant alleles are individually referred to as D, B and C, respectively. A coding region containing any of the D, B or C mutations is referred to as O, and the wild-type allele at each locus is referred to as A. The structural mutations impair triple helix formation in the MBL collagenous tail, leading to degradation and functional deficiency of MBL. Serum MBL concentrations are 10-20% of that expected in heterozygotes (A/O) for the structural polymorphisms, and virtually undetectable in functional homozygotes (O/O; individuals who are homozygous or doubly heterozygous for