Format

Send to

Choose Destination
Sci Rep. 2018 Jan 11;8(1):526. doi: 10.1038/s41598-017-18937-z.

Human complement receptor type 1 (CR1) protein levels and genetic variants in chronic Chagas Disease.

Author information

1
Laboratory of Molecular Immunopathology, Federal University of Paraná, Curitiba, Brazil.
2
Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
3
Faculty of Medicine, Duy Tan University, Da Nang, Vietnam.
4
Vietnamese - German Center for Medical Research, Hanoi, Vietnam.
5
Institute of Tropical Medicine, University of Tübingen, Tübingen, Germany. velavan@medizin.uni-tuebingen.de.
6
Faculty of Medicine, Duy Tan University, Da Nang, Vietnam. velavan@medizin.uni-tuebingen.de.
7
Vietnamese - German Center for Medical Research, Hanoi, Vietnam. velavan@medizin.uni-tuebingen.de.

Abstract

Complement is an essential element in both innate and acquired immunity contributing to the immunopathogenesis of many disorders, including Chagas Disease (CD). Human complement receptor 1 (CR1) plays a role in the clearance of complement opsonized molecules and may facilitate the entry of pathogens into host cells. Distinct CR1 exon 29 variants have been found associated with CR1 expression levels, increased susceptibility and pathophysiology of several diseases. In this study, CR1 plasma levels were assessed by ELISA and CR1 variants in exon 29 by sequencing in a Brazilian cohort of 232 chronic CD patients and 104 healthy controls. CR1 levels were significantly decreased in CD patients compared to controls (p < 0.0001). The CR1 rs1704660G, rs17047661G and rs6691117G variants were significantly associated with CD and in high linkage disequilibrium. The CR1*AGAGTG haplotype was associated with T. cruzi infection (p = 0.035, OR 3.99, CI 1.1-14.15) whereas CR1*AGGGTG was related to the risk of chagasic cardiomyopathy (p = 0.028, OR 12.15, CI 1.13-113). This is the first study that provides insights on the role of CR1 in development and clinical presentation of chronic CD.

PMID:
29323238
PMCID:
PMC5765048
DOI:
10.1038/s41598-017-18937-z
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center