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Review on Trypanosoma cruzi: Host Cell Interaction.

de Souza W, de Carvalho TM, Barrias ES - Int J Cell Biol (2010)

Bottom Line: Metacyclic trypomastigotes are released with the feces of the insect while amastigotes and bloodstream trypomastigotes are released from the infected host cells of the vertebrate host after a complex intracellular life cycle.The recognition between parasite and mammalian host cell involves numerous molecules present in both cell types.Here, we present a brief review of the interaction between Trypanosoma cruzi and its host cells, mainly emphasizing the mechanisms and molecules that participate in the T. cruzi invasion process of the mammalian cells.

View Article: PubMed Central - PubMed

Affiliation: Laboratório de Ultraestrutura Celular Hertha Meyer, CCS, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Bloco G, Ilha do Fundão, RJ 21941-902, Brazil.

ABSTRACT
Trypanosoma cruzi, the causative agent of Chagas' disease, which affects a large number of individuals in Central and South America, is transmitted to vertebrate hosts by blood-sucking insects. This protozoan is an obligate intracellular parasite. The infective forms of the parasite are metacyclic and bloodstream trypomastigote and amastigote. Metacyclic trypomastigotes are released with the feces of the insect while amastigotes and bloodstream trypomastigotes are released from the infected host cells of the vertebrate host after a complex intracellular life cycle. The recognition between parasite and mammalian host cell involves numerous molecules present in both cell types. Here, we present a brief review of the interaction between Trypanosoma cruzi and its host cells, mainly emphasizing the mechanisms and molecules that participate in the T. cruzi invasion process of the mammalian cells.

No MeSH data available.


Related in: MedlinePlus

Model of T. cruzi invasion. The model indicates three distinct mechanisms of T. cruzi entry into host cell. (a) the lysosome-dependent pathway is initiated by targeted Ca2+-regulated exocytosis of lysosomes in the plasma membrane; (b) in the actin dependent pathway trypomastigotes penetrate into a host cell through a plasma membrane expansion that culminates in assembly of a parasitophorous vacuole. Either learly endosomes or lysosomes can fuse with the parasitophorous vacuole; (c) in the lysosome-independent pathway, parasites enter cells through plasma membrane invaginations that accumulate PIP3 (product of class I PI3K activation). Subsequently, internalized parasites are contained in vacuoles formed from the plasma membrane and it maturates with the acquisition of early endosome markers (rab5 and EEA1) and subsequently with the acquisition of lysosome markers. Later on, the the trypomastigote form gradually transform into a amastigote form with simultaneous lysis of the parasitophorous vacuole membrane. Then, amastigotes in direct contact with the cytoplasm start to divide.
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Related In: Results  -  Collection


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fig10: Model of T. cruzi invasion. The model indicates three distinct mechanisms of T. cruzi entry into host cell. (a) the lysosome-dependent pathway is initiated by targeted Ca2+-regulated exocytosis of lysosomes in the plasma membrane; (b) in the actin dependent pathway trypomastigotes penetrate into a host cell through a plasma membrane expansion that culminates in assembly of a parasitophorous vacuole. Either learly endosomes or lysosomes can fuse with the parasitophorous vacuole; (c) in the lysosome-independent pathway, parasites enter cells through plasma membrane invaginations that accumulate PIP3 (product of class I PI3K activation). Subsequently, internalized parasites are contained in vacuoles formed from the plasma membrane and it maturates with the acquisition of early endosome markers (rab5 and EEA1) and subsequently with the acquisition of lysosome markers. Later on, the the trypomastigote form gradually transform into a amastigote form with simultaneous lysis of the parasitophorous vacuole membrane. Then, amastigotes in direct contact with the cytoplasm start to divide.

Mentions: The trypomastigotes which started a process of differentiation into amastigotes, while they are still located inside the PV during its membrane fragmentation was observed by transmission electron microscopy around 2 hours after infection [8]. In Figure 10, we have a scheme that sinthesized the mechanisms used by trypomastigotes to start an infection in a host cell.


Review on Trypanosoma cruzi: Host Cell Interaction.

de Souza W, de Carvalho TM, Barrias ES - Int J Cell Biol (2010)

Model of T. cruzi invasion. The model indicates three distinct mechanisms of T. cruzi entry into host cell. (a) the lysosome-dependent pathway is initiated by targeted Ca2+-regulated exocytosis of lysosomes in the plasma membrane; (b) in the actin dependent pathway trypomastigotes penetrate into a host cell through a plasma membrane expansion that culminates in assembly of a parasitophorous vacuole. Either learly endosomes or lysosomes can fuse with the parasitophorous vacuole; (c) in the lysosome-independent pathway, parasites enter cells through plasma membrane invaginations that accumulate PIP3 (product of class I PI3K activation). Subsequently, internalized parasites are contained in vacuoles formed from the plasma membrane and it maturates with the acquisition of early endosome markers (rab5 and EEA1) and subsequently with the acquisition of lysosome markers. Later on, the the trypomastigote form gradually transform into a amastigote form with simultaneous lysis of the parasitophorous vacuole membrane. Then, amastigotes in direct contact with the cytoplasm start to divide.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2926652&req=5

fig10: Model of T. cruzi invasion. The model indicates three distinct mechanisms of T. cruzi entry into host cell. (a) the lysosome-dependent pathway is initiated by targeted Ca2+-regulated exocytosis of lysosomes in the plasma membrane; (b) in the actin dependent pathway trypomastigotes penetrate into a host cell through a plasma membrane expansion that culminates in assembly of a parasitophorous vacuole. Either learly endosomes or lysosomes can fuse with the parasitophorous vacuole; (c) in the lysosome-independent pathway, parasites enter cells through plasma membrane invaginations that accumulate PIP3 (product of class I PI3K activation). Subsequently, internalized parasites are contained in vacuoles formed from the plasma membrane and it maturates with the acquisition of early endosome markers (rab5 and EEA1) and subsequently with the acquisition of lysosome markers. Later on, the the trypomastigote form gradually transform into a amastigote form with simultaneous lysis of the parasitophorous vacuole membrane. Then, amastigotes in direct contact with the cytoplasm start to divide.
Mentions: The trypomastigotes which started a process of differentiation into amastigotes, while they are still located inside the PV during its membrane fragmentation was observed by transmission electron microscopy around 2 hours after infection [8]. In Figure 10, we have a scheme that sinthesized the mechanisms used by trypomastigotes to start an infection in a host cell.

Bottom Line: Metacyclic trypomastigotes are released with the feces of the insect while amastigotes and bloodstream trypomastigotes are released from the infected host cells of the vertebrate host after a complex intracellular life cycle.The recognition between parasite and mammalian host cell involves numerous molecules present in both cell types.Here, we present a brief review of the interaction between Trypanosoma cruzi and its host cells, mainly emphasizing the mechanisms and molecules that participate in the T. cruzi invasion process of the mammalian cells.

View Article: PubMed Central - PubMed

Affiliation: Laboratório de Ultraestrutura Celular Hertha Meyer, CCS, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Bloco G, Ilha do Fundão, RJ 21941-902, Brazil.

ABSTRACT
Trypanosoma cruzi, the causative agent of Chagas' disease, which affects a large number of individuals in Central and South America, is transmitted to vertebrate hosts by blood-sucking insects. This protozoan is an obligate intracellular parasite. The infective forms of the parasite are metacyclic and bloodstream trypomastigote and amastigote. Metacyclic trypomastigotes are released with the feces of the insect while amastigotes and bloodstream trypomastigotes are released from the infected host cells of the vertebrate host after a complex intracellular life cycle. The recognition between parasite and mammalian host cell involves numerous molecules present in both cell types. Here, we present a brief review of the interaction between Trypanosoma cruzi and its host cells, mainly emphasizing the mechanisms and molecules that participate in the T. cruzi invasion process of the mammalian cells.

No MeSH data available.


Related in: MedlinePlus