Interactions of human galectins with Trypanosoma cruzi: binding profile correlate with genetic clustering of lineages.

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.