Background: Trypanosoma cruzi is the etiological agent of Chagas disease, a debilitating illness that affects millions of people in the Americas. A major finding of the T. cruzi genome project was the discovery of a novel multigene family composed of approximately 1,300 genes that encode mucin-associated surface proteins (MASPs). The high level of polymorphism of the MASP family associated with its localization at the surface of infective forms of the parasite suggests that MASP participates in host-parasite interactions. We speculate that the large repertoire of MASP sequences may contribute to the ability of T. cruzi to infect several host cell types and/or participate in host immune evasion mechanisms.
Methods: By sequencing seven cDNA libraries, we analyzed the MASP expression profile in trypomastigotes derived from distinct host cells and after sequential passages in acutely infected mice. Additionally, to investigate the MASP antigenic profile, we performed B-cell epitope prediction on MASP proteins and designed a MASP-specific peptide array with 110 putative epitopes, which was screened with sera from acutely infected mice.
Findings And Conclusions: We observed differential expression of a few MASP genes between trypomastigotes derived from epithelial and myoblast cell lines. The more pronounced MASP expression changes were observed between bloodstream and tissue-culture trypomastigotes and between bloodstream forms from sequential passages in acutely infected mice. Moreover, we demonstrated that different MASP members were expressed during the acute T. cruzi infection and constitute parasite antigens that are recognized by IgG and IgM antibodies. We also found that distinct MASP peptides could trigger different antibody responses and that the antibody level against a given peptide may vary after sequential passages in mice. We speculate that changes in the large repertoire of MASP antigenic peptides during an infection may contribute to the evasion of host immune responses during the acute phase of Chagas disease.
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http://dx.doi.org/10.1371/journal.pntd.0001779 | DOI Listing |
Braz J Vet Med
January 2025
Veterinarian, DSc, DMCV, IV, UFRRJ, Seropédica RJ, Brazil.
Canine heartworm disease causes significant pulmonary abnormalities, even in asymptomatic cases. This study aimed to compare the chest radiographs of cases infected with with those of heartworm-negative dogs. Fifteen animals treated at a private veterinary clinic in the municipality of Maricá, Rio de Janeiro, underwent chest radiography, regardless of their serological status, for the presence of antigen, and none of them used preventive measures.
View Article and Find Full Text PDFCogn Behav Ther
November 2024
TSET Health Promotion Research Center, Stephenson Cancer Center, University of Oklahoma Health Sciences Center, 655 Research Parkway, Oklahoma City, OK, USA.
Eur J Immunol
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Department of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
The alternative pathway (AP) plays a major role in many complement-mediated human diseases. Factor D (FD), a rate-limiting enzyme in AP complement activation, is an attractive therapeutic target. Unlike other complement proteins, FD is synthesized primarily in adipose tissue, and its levels in human blood are relatively low.
View Article and Find Full Text PDFJ Inflamm Res
October 2024
Department of Nephrology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215006, People's Republic of China.
Endosc Int Open
October 2024
Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kyoto, United States.
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