Table 1.
Demographic data and clinical parameters of Chagas patients.
Table 2.
Distribution of MBL2 alleles and haplotypes in patients and controls.
Fig 1.
Distribution of MBL levels according to MBL2 genotypes in controls and patients.
Open circles indicate individuals with the LYQC haplotype. Medians in each group are given by a horizontal line. P values refer to Kruskal-Wallis test.
Fig 2.
Distribution of MBL levels according to the functional classification of heart failure.
Open circles indicate patients with the YO haplotype; open diamonds, patients with the XA/XA or XA/YA genotypes. Medians in each group are given by a horizontal line. MBL levels were not analyzed in patients classified within the “B2” class. P value refers to Kruskal-Wallis test.
Table 3.
MBL2 genotype distribution according to functional classification of heart failure.
Fig 3.
Distribution of cytokine/chemokine levels according to the presence of MBL2*O (B, C or D) alleles.
A. IL9 distribution (P value refers to Mann-Whitney test; horizontal line indicates the median level). B. PDGF distribution (P value refers to an unpaired t-test; horizontal line indicates the mean level). C. RANTES distribution (P value refers to Mann-Whitney test; horizontal line indicates the median level). There were no MBL2*O/O homozygotes among those measured for the investigated cytokines/chemokines. Three outliers with inconsistent results were excluded from all comparisons. Due to small sample size, Bonferroni P values were not significant.
Fig 4.
Hypothetical role of high MBL levels in heart Chagas disease.
In the acute stage of T. cruzi infection, MBL molecules function as opsonins for the pathogen. Thus high MBL levels would increase phagocytosis of the parasite. In the chronic stage of the disease, MBL may bind to altered-cell molecular patterns expressed on myocardium of CD patients, activating the lectin pathway and leading to an increased secretion of RANTES and pro-inflammatory cytokines such as IL-9 and PDGF (in patients with the MBL2*A/A genotype), thereby promoting heart damage leading to chagasic chronic cardiomiopathy.