Abstract
The presence of the single nucleotide polymorphisms in exon 1 of the mannose-binding lectin 2 (MBL2) gene was evaluated in a sample of 159 patients undergoing coronary artery bypass surgery (71 patients undergoing valve replacement surgery and 300 control subjects) to investigate a possible association between polymorphisms and heart disease with Chlamydia infection. The identification of the alleles B and D was performed using real time polymerase chain reaction (PCR) and of the allele C was accomplished through PCR assays followed by digestion with the restriction enzyme. The comparative analysis of allelic and genotypic frequencies between the three groups did not reveal any significant difference, even when related to previous Chlamydia infection. Variations in the MBL plasma levels were influenced by the presence of polymorphisms, being significantly higher in the group of cardiac patients, but without representing a risk for the disease. The results showed that despite MBL2 gene polymorphisms being associated with the protein plasma levels, the polymorphisms were not enough to predict the development of heart disease, regardless of infection with both species of Chlamydia.
Highlights
Several infectious agents represent important risk factors in the development of atherosclerosis [1,2]; among them, Chlamydia pneumoniae in endothelial tissue has been strongly associated with coronary artery disease (CAD) [3,4,5,6]
We investigated the possible association between the presence of mannose-binding lectin 2 (MBL2) gene exon 1 mutations and previous infections with two species of Chlamydia in the predisposition for the development of cardiovascular disease
Variations in the promoter region associated with variations in the MBL2 gene exon 1 predictive of lower Mannose-binding lectin (MBL) levels were significantly related to CAD, regardless of other risk factors [18]
Summary
Several infectious agents represent important risk factors in the development of atherosclerosis [1,2]; among them, Chlamydia pneumoniae in endothelial tissue has been strongly associated with coronary artery disease (CAD) [3,4,5,6]. Mannose-binding lectin (MBL) is an important serum protein related to the innate immunity It binds to mannose carbohydrates and N-acetyl glucosamine and is expressed by a wide variety of microorganisms, promoting opsonization, phagocytosis and activation of the complement system [9,10]. The MBL*B, MBL*C and MBL*D alleles represent changes in codons 54 (Gli54Asp; SNP ID rs1800450), 57 (Gli57Glu; SNP ID rs1800451) and 52 (Arg52Cis; SNP ID rs5030737), respectively [13]. These mutations lead to structural changes in the protein, causing a functional deficiency and a significant reduction in the circulating MBL [14,15,16]. Variations in the MBL2 gene are responsible for poor opsonization and are associated with increased susceptibility to respiratory infections, including C. pneumoniae [17,18,19]
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