Parameters affecting cellular invasion and escape from the parasitophorous vacuole by different infective forms of Trypanosoma cruzi

The autophagic pathway is a key component in the lysosomal dependent entry ofTrypanosoma cruziinto the host cell

“…This is an interesting result taking into account that both strains have comparable enzymatic profiles. 47 Moreover, analyzing the parasite/Lamp-1 colocalization of T. cruzi CL Brener and RA strains, similar kinetics to LC3 association, were observed (data not shown). These results indicate that the interaction between T. cruzi and autophagosomes is transitory and does not seem to interrupt the normal fate of the parasite inside the host cell.…”

Mammalian cell invasion and intracellular trafficking by Trypanosoma cruzi infective forms

“…Cytoskeletal mutants of a melanoma cell line expressing varying amounts of actin binding protein 280, ABP280 (Cunningham et al 1992), a microfilament cross-linking protein, as well as NIH mouse fibroblasts expressing variable amounts of the actin assembly regulator protein gelsolin (Cunningham et al 1991) display distinct susceptibility towards metacyclic trypomastigotes or extracellular amastigotes of the G strain (Procópio et al 1998). We also observed that CHO cells with poorly sialylated proteins (Lec-2 cells, Deutscher et al 1984) are slightly more susceptible to extracellular amastigotes, when compared to the normal controls (Stecconi-Silva et al 2003). The observation that amastigotes and trypomastigotes become associated with distinct actinrich projections upon cell invasion prompted us to examine the role of regulatory Rho GTPases in this process.…”

“…This was true not only for Vero and HeLa cells (Mortara 1991, Procó-pio et al 1998) but also for the sialic acid mutant Lec-2 cells (Stecconi- Silva et al 2003). Of all target mammalian cells employed so far, only in the case of MDCK cells and the Rho transfectants, was metacyclic trypomastigotes infectivity higher than the corresponding extracellular amastigotes (see Table I and Fernandes and Mortara 2004).…”

“…Also, G strain metacyclics appear to mobilize intracellular calcium from acidocalcisomes whereas CL strain parasites preferentially use (1,4,5-inositol-triphosphate, IP 3 -dependent) endoplasmic reticulum stores during invasion (Neira et al 2002). Preliminary results from comparative studies between metacyclic trypomastigotes and extracellular amastigotes of the G strain, indicated that drugs that interfere with ER calcium mobilization (thapsigargin, A23187 ionophore) do not affect invasion of treated amastigotes (Stecconi- Silva et al 2003). Further analysis with other IP 3 -interfering compounds (caffeine, neomycin and U73122) confirmed that calcium mobilization in the parasite through IP 3 mobilization is not relevant for cellular invasion by extracellular amastigotes of either G or CL strains (Table I, Fernandes A.B., unpublished observations).…”

Acidotropic probes and flow cytometry: a powerful combination for detecting phagotrophy in mixotrophic and heterotrophic protists

“…Parasitophorous vacuoles, i.e. vacuoles that surround parasites (Antoine et al 1990, Maurin et al 1992, Stecconi-Silva et al 2003, are other acidic vesicles that can be stained by the acidotropic probes. Since parasitism is not rare among dinoflagellates (e.g.…”