The MASP family of Trypanosoma cruzi: changes in gene expression and antigenic profile during the acute phase of experimental infection.
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.


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.
Departamento de Parasitologia, Universidade Federal de Minas Gerais, Minas Gerais, Brazil.
Sara Lopes
SL
dos Santos
Leandro Martins
LM
Freitas
Francisco Pereira
FP
Lobo
Gabriela Flávia
GF
Rodrigues-Luiz
Tiago Antônio de Oliveira
TA
Mendes
Anny Carolline Silva
AC
Oliveira
Luciana Oliveira
LO
Andrade
Egler
E
Chiari
Ricardo Tostes
RT
Gazzinelli
Santuza Maria Ribeiro
SM
Teixeira
Ricardo Toshio
RT
Fujiwara
Daniella Castanheira
DC
Bartholomeu
D000818:Animals; D000913:Antibodies, Protozoan / Q000097:blood; D000953:Antigens, Protozoan / Q000096:biosynthesis / Q000276:immunology; D002460:Cell Line; D014355:Chagas Disease / Q000469:parasitology*; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000469:parasitology; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation; D006790:Host-Parasite Interactions; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D008565:Membrane Proteins / Q000096:biosynthesis / Q000276:immunology; D051379:Mice; D032446:Myoblasts / Q000469:parasitology; D015800:Protozoan Proteins / Q000096:biosynthesis* / Q000276:immunology; D014349:Trypanosoma cruzi / Q000235:genetics*
D000913:Antibodies, Protozoan; D000953:Antigens, Protozoan; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D008565:Membrane Proteins; D015800:Protozoan Proteins