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Background  In age-related macular degeneration (AMD) the complement system is thought to be activated by chronic oxidative damage with genetic variants identified in the alternative pathway as susceptibility factors. However, the involvement of the lectin pathway of complement, a key mediator of oxidative damage, is controversial. This study investigated whether mannose-binding lectin (MBL) levels and genetic variants in lectin pathway proteins, are associated with the predisposition to and severity of AMD.    Methods  MBL levels and single nucleotide polymorphisms (SNPs) in the  MBL2  and the ficolin-2 ( FCN2 ) gene were determined in 109 patients with AMD and 109 age- and sex-matched controls.    Results  MBL expression levels were equally distributed in both cases (early and late AMD) and controls (p>0.05). However, there was a trend towards higher median MBL levels in cases with late AMD compared to cases with early AMD (1.0 vs. 0.4 μg/ml, p = 0.09) and MBL deficiency (<0.5 μg/ml) was encountered less frequently in the late AMD group (35% vs 56%, p = 0.03).  FCN2  and  MBL2  allele frequencies were similarly distributed in early and late AMD cases compared with controls (p>0.05 for all analyses) as were  MBL2  genotypes. Similarly, there was no significant difference in allele frequencies in any SNPs in either the  MBL2  or  FCN2  gene in cases with early vs. late AMD.    Conclusions  SNPs of lectin pathway proteins investigated in this study were not associated with AMD or AMD severity. However, MBL levels deserve further study in a larger cohort of early vs. late AMD patients to elucidate any real effect on AMD severity.

plos one

Association Study of Mannose-Binding Lectin Levels and Genetic Variants in Lectin Pathway Proteins with Susceptibility to Age-Related Macular Degeneration: A Case-Control Study