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

Mortara, Renato Arruda; Procópio, Daniela O.; Barros, Helena C.; Verbisck, Newton V.; Andreoli, Walter K.; Silva, Ricardo Bs; Silva, Solange da

doi:10.1590/s0074-02761999000700014

Cited by 19 publications

(11 citation statements)

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“…It is interesting to note that the extracts of metacyclic trypomastigotes of either G or CL strains that express distinct repertoires of surface molecules related to their different infectivities are capable of inducing comparable levels of intracellular calcium transient raises in HeLa cells (Ruiz et al 1998), similar to what has been observed here for EA of the same strains. In a previous work, we found that EA from T. cruzi I strains are typically more infective than T. cruzi II parasites (Mortara et al 1999;Fernandes and Mortara 2004). The amastigote surface component(s) that trigger the HeLa cell calcium oscillations observed here have not yet been identified but preliminary evidences indicate that a carbohydrate epitope defined by a monoclonal antibody designated 1D9, abundant in T. cruzi I amastigotes (Barros et al 1997;Mortara et al 1999), could be implicated in this process.…”

Section: Hela Cell Calcium Transients Triggered By T Cruzi Extracellmentioning

confidence: 57%

“…In a previous work, we found that EA from T. cruzi I strains are typically more infective than T. cruzi II parasites (Mortara et al 1999;Fernandes and Mortara 2004). The amastigote surface component(s) that trigger the HeLa cell calcium oscillations observed here have not yet been identified but preliminary evidences indicate that a carbohydrate epitope defined by a monoclonal antibody designated 1D9, abundant in T. cruzi I amastigotes (Barros et al 1997;Mortara et al 1999), could be implicated in this process.…”

Section: Hela Cell Calcium Transients Triggered By T Cruzi Extracellmentioning

confidence: 57%

“…The efficiency in entering non-phagocytic mammalian cells may vary widely between T. cruzi strains and strains belonging to different phylogenetic lineages, and it has been well established that metacyclic trypomastigotes from CL strain (T. cruzi II) are highly invasive whereas parasites from the G strain (belonging to T. cruzi I) are poorly infective (Neira et al 2002). However, EA of highly infective strains such as Y and CL are poorly infective when compared to type I parasites, particularly from the G strain, showing the opposite behavior of the corresponding metacyclic trypomastigote forms (Mortara et al 1999;Fernandes and Mortara 2004). For metacyclic trypomastigotes, the developmental forms that initiate infection in mammalian hosts, the variability between these strains has been associated to the differential expression of surface glycoproteins that bind to target cells in a receptormediated manner and exhibit differential Ca 2+ signaling activities (Ruiz et al 1998;Yoshida et al 2000).…”

Section: Introductionmentioning

confidence: 99%

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Cell invasion by Trypanosoma cruzi amastigotes of distinct infectivities: studies on signaling pathways

et al. 2006

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Trypanosoma cruzi metacyclic trypomastigotes of the major phylogenetic lineages use specific signaling pathways to invade host cells. Using a panel of drugs, we studied if the differences in the ability of extracellular amastigotes (EA) from G (T. cruzi I) and CL (T. cruzi II) strains to invade host cells could be associated to activation of specific signaling routes. Sonicated extracts from G or CL strain EA induced transient raises in HeLa cell intracellular Ca(2+) levels in a dose-dependent manner. Treatment of EA with drugs that affect Ca(2+) release from inositol-1,4,5-triphosphate-sensitive stores did not significantly affect the infectivity of either strain, whereas EA of both strains treated with ionomycin plus NH(4)Cl or nigericin that release Ca(2+) from acidocalcisomes had their infectivity reduced. Treatment of parasites with adenylate cyclase activator forskolin increased the infectivity of both strains towards HeLa cells. These data, taken together, suggest that, for host cell invasion, G and CL strain EA engage signaling pathways that lead to an increase of cyclic adenosine monophosphate and Ca(2+) mobilization from acidocalcisomes. Moreover, treatment of EA with genistein reduced by approximately 45% the invasion of HeLa cells by G but not by CL strain, implicating a protein tyrosine kinase in the process. In line with this, HeLa cell extracts contained a protein tyrosine kinase activity that mediated the phosphorylation of 87- and 175-kDa polypeptides of EA from G but not from CL strain. Regarding the target cell response, the activation of host PI3 kinase appears to be required for invasion by either strain as treatment of HeLa cells with wortmannin reduced EA infectivity. These data overall reinforce the concept that cell invasion by T. cruzi EA markedly differs from the process involving metacyclic trypomastigotes.

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Section: Hela Cell Calcium Transients Triggered By T Cruzi Extracellmentioning

confidence: 57%

Section: Hela Cell Calcium Transients Triggered By T Cruzi Extracellmentioning

confidence: 57%

Section: Introductionmentioning

confidence: 99%

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Cell invasion by Trypanosoma cruzi amastigotes of distinct infectivities: studies on signaling pathways

et al. 2006

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“…Studies carried out by several groups have shown that involvement of host cell actin with cytochalasins interferes with the internalization of trypomastigote forms into vertebrate cells (Barbosa et al, 1995;Burleigh et al, 1995;Burleigh et al, 1998;Caler et al, 2000;Carvalho et al, 1999;Mortara et al, 1999;Nogueira et al, 1976;Procopio et al, 1994;Schenkman et al, 1991). In most of the studies such interference is negative, decreasing the rate of infection and increasing attachment (Barbosa et al, 1995;Meirelles et al, 1982).…”

Section: Discussionmentioning

confidence: 99%

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

Rosestolato

Dutra

Souza

et al. 2002

Cell Struct. Funct.

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ABSTRACT. The involvement of actin filaments from the host cell on the process of invasion of trypomastigote forms of Trypanosma cruzi was analyzed in seven different cell lines. Prior incubation of all cell lines with cytochalasin D, under conditions which interfere with actin filaments, markedly inhibited parasite internalization and increased parasite attachment. Attached parasites were readily ingested following washing of the drug-treated cells. Cytochalasin treatment interfered with the distribution of actin filaments of the host cell as evaluated by visualization of the filaments using confocal laser scanning microscopy of cells incubated in the presence of FITCphalloidin. Concentration of actin filaments could be observed in most, but not all, parasites in the process of internalization. We also treated LLCMK 2 and macrophage cells with Jasplakinolide, a drug that stabilizes actin filaments, before interaction with the trypomastigote forms. This drug partially inhibits parasite invasion into the cells. Prior incubation of the host cells in the presence of colchicine, which interfere with microtubules, also inhibited parasite internalization into the cells.

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“…Both the dividing amastigotes [60] and insect stage epimastigotes [61] are fully capable of establishing infections, and amastigotes are increasingly recognized to share comparable infectivity to trypomastigotes. Amastigote cell entry may follow more stereotyped pattern of cell invasion than the relatively diverse patterns noted between trypomastigotes and their targets.…”

Section: Cell Invasionmentioning

confidence: 99%

Molecular mechanisms of host cell invasion by Trypanosoma cruzi

Epting

Coates

Engman

2010

Experimental Parasitology

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The protozoan parasite Trypanosoma cruzi, the etiologic agent of Chagas disease, is an obligate intracellular protozoan pathogen. Overlapping mechanisms ensure successful infection, yet the relationship between these cellular events and clinical disease remains obscure. This review explores the process of cell invasion from the perspective of cell surface interactions, intracellular signaling, modulation of the host cytoskeleton and endosomal compartment, and the intracellular innate immune response to infection.

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

Abstract: Through its life cycle from the insect vector to mammalian hosts

Cited by 19 publications

References 19 publications

Cell invasion by Trypanosoma cruzi amastigotes of distinct infectivities: studies on signaling pathways

Cell invasion by Trypanosoma cruzi amastigotes of distinct infectivities: studies on signaling pathways

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

Molecular mechanisms of host cell invasion by Trypanosoma cruzi

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