Trypanosoma cruzi: Effect of Protein Kinase Inhibitors and Cytoskeletal Protein Organization and Expression on Host Cell Invasion by Amastigotes and Metacyclic Trypomastigotes

Features of host cell invasion by different infective forms of Trypanosoma cruzi

“…We observed that amastigotes normally displayed a higher capability of invasion on most cells. The effect of drugs that interfere with microfilament (cytochalasin D) or microtubule (nocodazole) assembly on the invasion of the two infective forms was also not only cell (HeLa or Vero) but also infective form dependent (Procópio et al 1998).…”

“…Drugs that interfere with protein phosphorylation (genistein and staurosporine) also displayed contrasting effects (Procópio et al 1998).…”

“…The recruitment of extracellular matrix components of HeLa and Vero cells, their integrin receptors and cytoskeletal elements was examined under electron and confocal fluorescence microscopy and significant differences were again found in the pattern involving either trypomastigote or extracellular amastigote invasion (Procópio et al 1998).…”

A century of research: what have we learned about the interaction of Trypanosoma cruzi with host cells?

“…Trypomastigotes that use this route mobilise phosphorylated inositides during the formation of the PV. These molecules then mature and become enriched in the same compartments as the lysosomal marker L�MP-1 (Tardieux et al 1992, Procópio et al 1998, Woolsey et al 200�, �ndrade & �ndrews 2004. One important outcome of this work was to demonstrate for the first time the relative contributions of each mode of entry, namely PI�-K (50%), lysosome (20%) and endosomal routes (20%) (Woolsey et al 200�).…”

“…The relative roles of PI�-K, en-. The relative roles of PI�-K, endosomal trafficking and L�MP-1 (Procópio et al 1998) pathways in extracellular amastigote invasion are still not fully understood.…”