Actin-rich structures formed during the invasion of cultured cells by infective forms of Trypanosoma cruzi

Novel PI 3-kinase-dependent mechanisms of trypanosome invasion and vacuole maturation

“…While the existence of an actin-associated pathway for T. cruzi invasion of nonprofessional phagocytic cells has also been suggested (Procopio et al, 1999;Rosestolato et al, 2002), we find that F-actin co-localization with invading trypomastigotes is minimal and that envelopment of infective T. cruzi trypomastigotes in a confined plasma membrane-derived vacuole does not require host cell actin polymerization. On the contrary, the overall capacity for cell invasion by T. cruzi is enhanced by cytochalasin D pretreatment, in support of previous reports (Tardieux et al, 1992;Rodriguez et al, 1995;Kima et al, 2000).…”

AFAP-1L1-mediated actin filaments crosslinks hinder Trypanosoma cruzi cell invasion and intracellular multiplication

“…Our results showed that decreased expression of AFAP-1L1, favored intracellular parasite invasion (Figure 1 B, C). The consensus in the field is that TCT actively invade cells and that the cortical actin filaments hinder cell invasion since their disruption facilitates the process (Mortara, 1991;Procópio et al, 1999;Mortara et al, 2007). Our results supported the consensus and also provided evidences that AFAP-1L1 may play important role in stabilizing actin filaments.…”

“…Along the past decades, authors have attempted to understand the molecular mechanisms beneath T. cruzi mammalian cell internalization, intracellular traffic and multiplication. In this context, host endocytic pathway-related molecules (Dutra et al, 2005;Barrias et al, 2010;Teixeira et al, 2015), lisosome exocytosis with delivery of acid sphingomyelinase to the outer leaflet of the plasma membrane (Fernandes et al, 2011) and actin cytoskeleton polymerization have been shown to play important role (Woolsey and Burleigh, 2004;Fernandes et al, 2013;Barrias et al, 2012;Mott et al, 2009;Ferreira et al, 2006;Vieira et al, 2002;Procópio et al, 1999).…”

Cytoskeleton reassembly in cardiomyocytes infected by Trypanosoma cruzi is triggered by treatment with ergosterol biosynthesis inhibitors

“…However, the effect on cytoskeletal dynamics appears to be dependent on the infective form of the parasite [30][31][32] and the signalling transduction pathway [27,33,34]. Recruitment of actin filaments to the site where the infective forms of T. cruzi are found has been demonstrated [25,31], whilst depolymerisation of actin filaments and lysosome recruitment at the site of invasion have been reported in response to Ca 2+ signalling [26,35]. Furthermore, our previous data revealed that T. cruzi infection induces damage to the cardiomyocyte cytoarchitecture.…”