Anti-galectin-1 autoantibodies in human Trypanosoma cruzi infection: differential expression of this beta-galactoside-binding protein in cardiac Chagas' disease

The pathogenesis of Chagas' disease has been subject of active research and still remains to be ascertained. Galectin-1 (Gal-1), a member of a conserv ed family of animal beta -galactoside-binding proteins, localized in human heart tissue, has been suggested to play key roles in immunological and inf lammatory processes. In the present study we demonstrated the occurrence of anti-Gal-1 autoAb in sera from patients in the acute and chronic stages of Chagas' disease (ACD and CCD) by means of ELISA and Western blot analysis. We found a marked increase in the level and frequency of Ig E anti-Gal-1 a ntibodies in sera from patients with ACD, but a low frequency of Ig M anti- Gal-1 immunoreactivity. Moreover, Ig G immunoreactivity to this beta -galac toside-binding protein was found to be correlated with the severity of card iac damage in CCD, but was absent in nonrelated cardiomyopathies. We could not detect immunoreactivity with Trypanosoma cruzi antigens using a polyclo nal antibody raised to human Gal-1 and no hemagglutinating activity could b e specifically eluted from a lactosyl-agarose matrix from parasite lysates. Moreover, despite sequence homology between Gal-1 and shed acute phase ant igen (SAPA) of T. cruzi, anti-Gal-1 antibodies eluted from human sera faile d to cross-react with SAPA. In an attempt to explore whether Gal-1 immunore activity was originated from endogenous human Gal-1, we finally investigate d its expression levels in cardiac tissue (the main target of Chagas' disea se). This protein was found to be markedly upregulated in cardiac tissue fr om patients with severe CCD, compared to cardiac tissue from normal individ uals.