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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

Imunofluorescence microscopy localization of GM1 (a–d) and flotillin 1 (e-f) during internalization of T. cruzi trypomastigotes by macrophages suggests the participation of membrane microdomins in this process. (a–d) colocalization of GM1, using cholera toxin subunit B (a) and an intracellular parasite ((c): arrow). (b) shows labeling of the nucleus and kinetoplast labeled with propidium iodide. (c) corresponds to a DIC image; (d) is a merge image. (e-f): Colocalization of flotillin1 (a), detected using a specific antibody, and trypomastigotes ((b): arrows) bars – 5 μm (after [16]).
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fig4: Imunofluorescence microscopy localization of GM1 (a–d) and flotillin 1 (e-f) during internalization of T. cruzi trypomastigotes by macrophages suggests the participation of membrane microdomins in this process. (a–d) colocalization of GM1, using cholera toxin subunit B (a) and an intracellular parasite ((c): arrow). (b) shows labeling of the nucleus and kinetoplast labeled with propidium iodide. (c) corresponds to a DIC image; (d) is a merge image. (e-f): Colocalization of flotillin1 (a), detected using a specific antibody, and trypomastigotes ((b): arrows) bars – 5 μm (after [16]).

Mentions: Host cell plasma membrane microdomains were also shown to be involved in T. cruzi entry both in nonphagocytic and phagocytic cells [16, 100]. Both groups demonstrated that cholesterol, the major components of membrane rafts and molecular markers of this domain like flotillin1 colocalized with trypomastigote and amastigote entry sites, suggesting the participation of microdomains in Trypanosoma cruzi invasion (Figure 4).


Review on Trypanosoma cruzi: Host Cell Interaction.

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

Imunofluorescence microscopy localization of GM1 (a–d) and flotillin 1 (e-f) during internalization of T. cruzi trypomastigotes by macrophages suggests the participation of membrane microdomins in this process. (a–d) colocalization of GM1, using cholera toxin subunit B (a) and an intracellular parasite ((c): arrow). (b) shows labeling of the nucleus and kinetoplast labeled with propidium iodide. (c) corresponds to a DIC image; (d) is a merge image. (e-f): Colocalization of flotillin1 (a), detected using a specific antibody, and trypomastigotes ((b): arrows) bars – 5 μm (after [16]).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Imunofluorescence microscopy localization of GM1 (a–d) and flotillin 1 (e-f) during internalization of T. cruzi trypomastigotes by macrophages suggests the participation of membrane microdomins in this process. (a–d) colocalization of GM1, using cholera toxin subunit B (a) and an intracellular parasite ((c): arrow). (b) shows labeling of the nucleus and kinetoplast labeled with propidium iodide. (c) corresponds to a DIC image; (d) is a merge image. (e-f): Colocalization of flotillin1 (a), detected using a specific antibody, and trypomastigotes ((b): arrows) bars – 5 μm (after [16]).
Mentions: Host cell plasma membrane microdomains were also shown to be involved in T. cruzi entry both in nonphagocytic and phagocytic cells [16, 100]. Both groups demonstrated that cholesterol, the major components of membrane rafts and molecular markers of this domain like flotillin1 colocalized with trypomastigote and amastigote entry sites, suggesting the participation of microdomains in Trypanosoma cruzi invasion (Figure 4).

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