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

MedStar author(s):
Citation: PLoS ONE [Electronic Resource]. 14(1):e0210640, 2019.PMID: 30629683Institution: MedStar Health Research InstituteForm of publication: Journal ArticleMedline article type(s): Journal ArticleSubject headings: *Chlamydophila pneumoniae/me [Metabolism] | *Chlamydophila pneumoniae/py [Pathogenicity] | *Mannose-Binding Lectin/me [Metabolism] | Aged | Alleles | Cardiovascular Diseases/ge [Genetics] | Cardiovascular Diseases/me [Metabolism] | Cardiovascular Diseases/pa [Pathology] | Case-Control Studies | Chlamydophila pneumoniae/ge [Genetics] | Female | Genetic Predisposition to Disease/ge [Genetics] | Genotype | Humans | Indians, North American | Linkage Disequilibrium/ge [Genetics] | Male | Mannose-Binding Lectin/ge [Genetics] | Middle Aged | Polymorphism, Single Nucleotide/ge [Genetics] | Promoter Regions, Genetic/ge [Genetics]Year: 2019Local holdings: Available online through MWHC library: 2006 - presentISSN:
  • 1932-6203
Name of journal: PloS oneAbstract: 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.All authors: Anderson MZ, Best LG, DeCroo S, Monsey L, Zhu JFiscal year: FY2019Digital Object Identifier: ORCID: Date added to catalog: 2019-01-18
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Journal Article MedStar Authors Catalog Article 30629683 Available 30629683

Available online through MWHC library: 2006 - present

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.

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