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Genetically Determined MBL Deficiency Is Associated with Protection against Chronic Cardiomyopathy in Chagas Disease
Paola Rosa Luz1, Márcia I Miyazaki2, Nelson Chiminacio Neto3
1Laboratório de Imunopatologia Molecular-Departamento de Patologia Médica, Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, Brasil.
Insights
Genetic MBL deficiency protects against Chagas disease (CD). Individuals with MBL deficiency showed reduced heart damage and lower inflammatory markers, suggesting a protective role in CD cardiomyopathy.
Area of Science:
- Immunology
- Genetics
- Infectious Diseases
Background:
- Chagas disease (CD) is caused by Trypanosoma cruzi.
- Mannan-binding lectin (MBL) recognizes parasite sugars and activates complement.
- MBL levels are influenced by MBL2 gene polymorphisms.
Purpose of the Study:
- Investigate the association between MBL2 gene polymorphisms and Chagas disease.
- Determine the role of MBL deficiency in CD development and progression, particularly cardiomyopathy.
Main Methods:
- Sequencing of the MBL2 promoter and exon 1 in 196 CD patients and 202 controls.
- Statistical analysis to assess the association between MBL2 alleles, MBL deficiency, and disease phenotypes.
- Measurement of cytokine and chemokine levels in patients.
Main Results:
- The MBL2*C allele, causing MBL deficiency, was associated with protection against CD.
- Genotypes with MBL deficiency were absent in patients with cardiac CD.
- MBL deficiency correlated with less heart damage and lower levels of specific cytokines/chemokines (IL9, PDGFB, RANTES).
Conclusions:
- Genetically determined MBL deficiency appears to offer protection against Chagas disease.
- MBL deficiency may prevent or slow the progression of chronic CD cardiomyopathy.
- This suggests MBL levels as a potential factor in Chagas disease pathogenesis.
Abstract:
Chagas disease (CD) is caused by Trypanosoma cruzi, whose sugar moieties are recognized by mannan binding lectin (MBL), a soluble pattern-recognition molecule that activates the lectin pathway of complement. MBL levels and protein activity are affected by polymorphisms in the MBL2 gene. We sequenced the MBL2 promoter and exon 1 in 196 chronic CD patients and 202 controls. The MBL2*C allele, which causes MBL deficiency, was associated with protection against CD (P = 0.007, OR = 0.32). Compared with controls, genotypes with this allele were completely absent in patients with the cardiac form of the disease (P = 0.003). Furthermore, cardiac patients with genotypes causing MBL deficiency presented less heart damage (P = 0.003, OR = 0.23), compared with cardiac patients having the XA haplotype causing low MBL levels, but fully capable of activating complement (P = 0.005, OR = 7.07). Among the patients, those with alleles causing MBL deficiency presented lower levels of cytokines and chemokines possibly implicated in symptom development (IL9, p = 0.013; PDGFB, p = 0.036 and RANTES, p = 0.031). These findings suggest a protective effect of genetically determined MBL deficiency against the development and progression of chronic CD cardiomyopathy.
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