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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

Transmission electron microscopy (TEM) of thin sections of macrophages infected with trypomastigote forms of T. cruzi. Micrographs taken at different inclination angles of the section. Focal disruption of the membrane lining the vacuole is observed (arrows in (a) and (b)) and especially in (c) and (d);  K = kinetoplast, P = parasite. Bars = 1 μm (after [52]).
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fig9: Transmission electron microscopy (TEM) of thin sections of macrophages infected with trypomastigote forms of T. cruzi. Micrographs taken at different inclination angles of the section. Focal disruption of the membrane lining the vacuole is observed (arrows in (a) and (b)) and especially in (c) and (d); K = kinetoplast, P = parasite. Bars = 1 μm (after [52]).

Mentions: Trypomastigote stages of T. cruzi use different receptor0073/linkers to get into host cells. Regardless of the mechanism used (either by fusion of lysosomes at the site of entry, by participation of components of the plasma membrane or by initial fusion with endosome compartments at the site of invasion), the parasite will be located in a vacuole. Studies show that some molecules are excluded when the vacuole is being formed. Some authors refer to the process of lysis of the PV membrane as an “escape” of the parasite from the parasitophorous vacuole. We prefer to characterize this process as a consequence of disintegration of the parasitophorous vacuole membrane. More studies are necessary to better characterize the mechanism involved in this important step of the T. cruzi life cycle. In the PV, trypomastigote forms release trans-sialidase/neuraminidase, that will remove sialic acid residues from the PV membrane making it sensitive to the action of Tc-Tox (a peptide that has homology with the factor 9 of the human complement) [111]. At the acidic pH of PV, this molecule will begin to destroy, maybe by pore formation, the PV membrane [8, 112, 113] (Figure 9). We suppose that the formation of these small pores, associated with the action of secreted enzymes, like transialidase/neuraminidase, by the parasite, will lead to the fragmentation of the PV membrane. Host cell treatment with drugs that raise the intracellular pH delayed the fragmentation of the PV membrane [114]. On the other hand, observations using CHO cells that are deficient in sialylation showed that the absence of sialic acid makes the PV membrane more sensitive to lysis [115]. The presence of sialic acid residues seems to protect the lysosome membrane from lysis.


Review on Trypanosoma cruzi: Host Cell Interaction.

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

Transmission electron microscopy (TEM) of thin sections of macrophages infected with trypomastigote forms of T. cruzi. Micrographs taken at different inclination angles of the section. Focal disruption of the membrane lining the vacuole is observed (arrows in (a) and (b)) and especially in (c) and (d);  K = kinetoplast, P = parasite. Bars = 1 μm (after [52]).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig9: Transmission electron microscopy (TEM) of thin sections of macrophages infected with trypomastigote forms of T. cruzi. Micrographs taken at different inclination angles of the section. Focal disruption of the membrane lining the vacuole is observed (arrows in (a) and (b)) and especially in (c) and (d); K = kinetoplast, P = parasite. Bars = 1 μm (after [52]).
Mentions: Trypomastigote stages of T. cruzi use different receptor0073/linkers to get into host cells. Regardless of the mechanism used (either by fusion of lysosomes at the site of entry, by participation of components of the plasma membrane or by initial fusion with endosome compartments at the site of invasion), the parasite will be located in a vacuole. Studies show that some molecules are excluded when the vacuole is being formed. Some authors refer to the process of lysis of the PV membrane as an “escape” of the parasite from the parasitophorous vacuole. We prefer to characterize this process as a consequence of disintegration of the parasitophorous vacuole membrane. More studies are necessary to better characterize the mechanism involved in this important step of the T. cruzi life cycle. In the PV, trypomastigote forms release trans-sialidase/neuraminidase, that will remove sialic acid residues from the PV membrane making it sensitive to the action of Tc-Tox (a peptide that has homology with the factor 9 of the human complement) [111]. At the acidic pH of PV, this molecule will begin to destroy, maybe by pore formation, the PV membrane [8, 112, 113] (Figure 9). We suppose that the formation of these small pores, associated with the action of secreted enzymes, like transialidase/neuraminidase, by the parasite, will lead to the fragmentation of the PV membrane. Host cell treatment with drugs that raise the intracellular pH delayed the fragmentation of the PV membrane [114]. On the other hand, observations using CHO cells that are deficient in sialylation showed that the absence of sialic acid makes the PV membrane more sensitive to lysis [115]. The presence of sialic acid residues seems to protect the lysosome membrane from lysis.

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