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Cardiovascular disease (CVD) is an important contributor to morbidity and mortality in American Indian communities. The Strong Heart Study (SHS) was initiated in response to the need for population based estimates of cardiovascular disease in American Indians. Previous studies within SHS have identified correlations between heart disease and deficiencies in mannose binding lectin (MBL), a motif recognition molecule of the innate immune system. MBL mediates the immune response to invading pathogens including  Chlamydia pneumoniae  ( Cp ), which has also been associated with the development and progression of CVD. However, a link between  MBL2  genotype and  Cp  in contributing to heart disease has not been established. To address this, SHS collected baseline  Cp  antibody titers (IgA and IgG) and  MBL2  genotypes for common functional variants from 553 individuals among twelve participating tribes. A single nucleotide polymorphism (SNP) in the promoter, designated X/Y, correlated significantly with increased  Cp  IgG titer levels, whereas another promoter SNP (H/L) did not significantly influence antibody levels to  Cp . Two variants within exon 1 of  MBL2 , the A and B alleles, also displayed significant association with  Cp  antibody titers. Some  MBL2  genotypes were absent from the population, suggesting linkage disequilibrium may be operating within the SHS cohort. Additional factors, such as increasing age and socioeconomic status, were also associated with increased  Cp  IgG antibody titers. This study demonstrates that  MBL2  genotype associates with immune reactivity to  C .  pneumoniae  in the SHS cohort. Thus,  MBL2  may contribute to the progression of cardiovascular disease (CVD) among American Indians indirectly through pathogen interactions in addition to its previously defined roles.

The association of mannose binding lectin genotype and immune response to Chlamydia pneumoniae: The Strong Heart Study