Participation of Host Cell Actin Filaments during Interaction of Trypomastigote Forms of Trypanosoma cruzi with Host Cells.

Rosestolato, Carlos Tadeu Fonseca; Dutra, Juliana da Matta Furniel; Souza, Wanderley de; Carvalho, Técia Maria Ulisses de

doi:10.1247/csf.27.91

Cited by 43 publications

(49 citation statements)

References 25 publications

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“…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).…”

Section: Discussioncontrasting

confidence: 40%

“…Coombes and Mahony, 2002), T. cruzi entry into a variety of non-professional phagocytic cells is significantly enhanced following disruption of the host cell actin cytoskeleton (Tardieux et al, 1992). While the universality of this concept has recently been challenged (Procipio et al, 1999;Rosestolato et al, 2002) these observations suggest that depolymerization of the cortical actin cytoskeleton (Rodriguez et al, 1995) in response to parasite-triggered Ca 2+ transients (Tardieux et al, 1994;Burleigh et al, 1997;Scharfstein et al, 2000) may enhance invasion by facilitating docking and fusion of lysosomes with the plasma membrane (Rodriguez et al, 1995;Tardieux et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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

Woolsey

Sunwoo

Petersen

et al. 2003

Journal of Cell Science

147

179

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Mammalian cell invasion by the protozoan parasite, Trypanosoma cruzi, is facilitated by the activation of host cell phosphatidylinositol 3 (PI 3)-kinases. We demonstrate that the well-characterized Ca2+-regulated lysosome-mediated parasite entry pathway is abolished by wortmannin pretreatment. In addition, we have characterized a novel route of T. cruzi invasion unexpectedly revealed in the course of this study. For over a decade, targeted exocytosis of lysosomes at the host cell plasma membrane was considered as the primary mechanism for T. cruzi entry into non-professional phagocytic cells. We now provide evidence that a significant fraction (50% or greater) of invading T. cruzi trypomastigotes exploit an alternate actin-independent entry pathway that involves formation of a tightly associated host cell plasma membrane-derived vacuole enriched in the lipid products of class I PI 3-kinases, PtdInsP3/PtdIns(3,4)P2. Initially devoid of lysosomal markers, the resultant parasite-containing vacuoles gradually acquire lysosome associated membrane protein 1 (lamp-1) and fluid phase endocytic tracer from the lysosomal compartment. In striking contrast to latex bead phagosomes, few T. cruzi vacuoles associate with the early endosomal marker, EEA1 and the 'maturation' process becomes refractory to PI 3-kinase inhibition immediately following parasite internalization. Jointly, these data provide a new paradigm for T. cruzi invasion of non-professional phagocytic cells and reveal a novel vacuole maturation process that appears to bypass the requirement for EEA1.

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Section: Discussioncontrasting

confidence: 40%

Section: Introductionmentioning

confidence: 99%

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

Woolsey

Sunwoo

Petersen

et al. 2003

Journal of Cell Science

147

179

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“…However, such an effect has not been detected by other groups. Cytochalasin D had little or no effect on TCT entry into MDCK or HeLa cells (Schenkman et al 1991c) whereas marked inhibiton was detected in diverse cell types, including Vero, LLCMK 2, HFSF fibrob-last, L-6 skeletal muscle myoblast and resident peritoneal macrophages (Rosestolato et al 2002), in addition to heart muscle cells (Barbosa and Meirelles 1995). As regards MT invasion, it was significantly inhibited by treatment of HeLa cells with cytochalasin B or latrunculin B (Osuna et al 1993), but unaffected by cytochalasin D (Schenkman and Mortara 1992).…”

Section: Host Cell Actin Cytoskeletonmentioning

confidence: 99%

Molecular basis of mammalian cell invasion by Trypanosoma cruzi

Yoshida

2006

An. Acad. Bras. Ciênc.

211

184

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Establishment of infection by Trypanosoma cruzi, the agent of Chagas´disease, depends on a series of events involving interactions of diverse parasite molecules with host components. Here we focus on the mechanisms of target cell invasion by metacyclic trypomastigotes (MT) and mammalian tissue culture trypomastigotes (TCT). During MT or TCT internalization, signal transduction pathways are activated both in the parasite and the target cell, leading to Ca 2+ mobilization. For cell adhesion, MT engage surface glycoproteins, such as gp82 and gp35/50, which are Ca 2+ signal-inducing molecules. In T. cruzi isolates that enter host cells in gp82-mediated manner, parasite protein tyrosine kinase as well as phospholipase C are activated, and Ca 2+ is released from IP 3 -sensitive stores, whereas in T. cruzi isolates that attach to target cells mainly through gp35/50, the signaling pathway involving adenylate cyclase appears to be stimulated, with Ca 2+ release from acidocalciosomes. In addition, T. cruzi isolate-dependent inhibitory signals, mediated by MT-specific gp90, may be triggered both in the host cell and the parasite. The repertoire of TCT molecules implicated in cell invasion includes surface glycoproteins of gp85 family, with members containing binding sites for laminin and cytokeratin 18, enzymes such as cruzipain, trans-sialidase, and an oligopeptidase B that generates a Ca 2+ -agonist from a precursor molecule.Key words: Trypanosoma cruzi, trypomastigotes, cell invasion, signal transduction, Ca 2+ mobilization. OVERVIEWTrypanosoma cruzi is transmitted by insect vectors when these blood-sucking triatomines deposit on the skin their feces containing MT, the infective forms of the parasite. Through the ocular mucosa or lesions in the skin, the parasites find their way to invade host cells. Metacyclic forms may enter mammalian hosts also by oral route. According to Coura et al. (2002), more than half of the acute cases of Chagas disease recorded between 1968 and 2000 in Brazilian Amazon can be attributed to microepidemics of orally E-mail: nyoshida@ecb.epm.br transmitted infection from contaminated food. The potential sources of contamination are whole triatomine insects or their feces containing infective parasites. Hoft (1996) has shown that MT are efficient in establishing infection in mice when given orally. They enter the gastric mucosal epithelium, transform into amastigotes and replicate intracellularly (Hoft et al. 1996) Mammalian cell invasion by T. cruzi has been extensively studied in vitro by using MT cultured in liquid media and TCT, as counterparts of insectborne and bloodstream parasites respectively. Different T. cruzi isolates and a variety of cell types, mostly cells that are not professional phagocytes, have been used (Table I). The picture emerging from these studies is that T. cruzi penetration into host cells is a multi-step process involving various parasite and host cell molecules that, in a concerted series of events, leads to intracellular Ca 2+ mobilization in both cells (Do...

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“…According to some authors, T. cruzi internalization is independent of the host cell actin cytoskeleton so that treatment of target cells with cytochalasin D, a drug that disrupts actin microfilaments, does not affect or increases parasite invasion (29,35). On the other hand, other authors have claimed that this drug has an inhibitory effect on T. cruzi entry into diverse cell types, including fibroblasts, skeletal muscle myoblasts, cardiomyocytes, and resident peritoneal macrophages (3,24). This discrepancy, observed in experiments with tissue culture trypomastigotes (TCT), extends to metacyclic trypomastigotes, the developmental forms that in natural infections are responsible for the first T. cruzi interaction with host cells.…”

mentioning

confidence: 99%

Actin Cytoskeleton-Dependent and -Independent Host Cell Invasion byTrypanosoma cruziIs Mediated by Distinct Parasite Surface Molecules

et al. 2006

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The disassembly of host cell actin cytoskeleton as a facilitator of Trypanosoma cruzi invasion has been reported by some authors, while other workers claim that it instead inhibits internalization of the parasite. In this study we aimed at elucidating the basis of this discrepancy. We performed experiments with metacyclic trypomastigotes of T. cruzi strains G and CL, which differ markedly in infectivity and enter target cells by engaging the surface molecules gp35/50 and gp82, respectively, which have signaling activity. Treatment of HeLa cells with the F-actin-disrupting drug cytochalasin D or latrunculin B inhibited the invasion by strain G but not the invasion by strain CL. In contrast to cells penetrated by strain CL, which were previously shown to have a disrupted actin cytoskeleton architecture, no such alteration was observed in HeLa cells invaded by strain G, and parasites were found to be closely associated with target cell actin. Coinfection with enteroinvasive Escherichia coli (EIEC), which recruits host cell actin for internalization, drastically reduced entry of strain CL into HeLa cells but not entry of strain G. In contrast to gp82 in its recombinant form, which induces disruption of F-actin and inhibits EIEC invasion, purified mucin-like gp35/50 molecules promoted an increase in EIEC uptake by HeLa cells. These data, plus the finding that drugs that interfere with mammalian cell signaling differentially affect the internalization of metacyclic forms of strains G and CL, indicate that the host cell invasion mediated by gp35/50 is associated with signaling events that favor actin recruitment, in contrast to gp82-dependent invasion, which triggers the signaling pathways leading to disassembly of F-actin.

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Participation of Host Cell Actin Filaments during Interaction of Trypomastigote Forms of Trypanosoma cruzi with Host Cells.

Cited by 43 publications

References 25 publications

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

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

Molecular basis of mammalian cell invasion by Trypanosoma cruzi

Actin Cytoskeleton-Dependent and -Independent Host Cell Invasion byTrypanosoma cruziIs Mediated by Distinct Parasite Surface Molecules

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