We report here the specific interaction between several members of the human
galectin family with the three developmental stages of several genetic lineages of the protozoan parasite Trypanosoma cruzi. We provide data of specific and differential binding of human
galectin (gal)-1, -3, -4, -7 and -8 to 14 strains of T. cruzi that belong to the six genetic lineages representing the genetic diversity of the parasite. It is shown that
galectins preferentially bind forms present in the host, trypomastigotes and amastigotes, compared with the non-infective epimastigote present on the intestinal tract of the vector, reflecting the changes on glycosylation that occur during the metacyclogenesis and amastigogenesis process. Also, it is evidenced that
galectin binding to the parasites promotes binding to the host cells and higher
infection rates. In addition, evidence is provided indicating that the intracellular amastigotes may take over the cytosolic pool of some
galectins when released to the extracellular medium. Finally, by applying unweighted pair group method analysis to the
galectin-binding profile to either cell-derived trypomastigotes or amastigotes, we show that the differential-binding profile by the host
galectins to the six lineages resembles the clustering based in genetic data. Therefore, the differential-binding profile for the six lineages could have implications in the immunopathology of
Chagas' disease, affecting the complex network of immune responses on which
galectins mediate, thus providing linkage clues to the notion that different lineages may be related to different clinical forms of the disease.