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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

Life cycle of T. cruzi showing the various forms of the protozoan in the invertebrate (triatomines) and vertebrate (mammals) hosts. Figure reproduced from the Center of Control Diseases homepage.
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Related In: Results  -  Collection


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fig1: Life cycle of T. cruzi showing the various forms of the protozoan in the invertebrate (triatomines) and vertebrate (mammals) hosts. Figure reproduced from the Center of Control Diseases homepage.

Mentions: One specific feature of the trypanosomatids is that they change their general shape during their life cycle. In those species that switch from vertebrate to invertebrate hosts, this and other changes may be dramatic, involving the appearance of developmental stages which do not divide and stages which are highly infective through a process generally described as protozoan differentiation or transformation [1, 2]. Among the trypanosomatids, T. cruzi presents one of the most complex life cycles involving several developmental stages found in the vertebrate and the invertebrate hosts as well as in the bloodstream and within vertebrate host cells. Figure 1 shows a general view of the life cycle of this protozoan. Let us consider that the cycle starts with insects from the Reduviidae family sucking the blood of vertebrates infected with the trypomastigote forms which circulate in the bloodstream (known as bloodstream trypomastigotes). Once ingested, most of the trypomastigotes are lysed in the insect's stomach [3]. The surviving trypomastigotes transform, in a few days later, either into spherical stage (known as spheromastigotes) or into epimastigote stage. Epimastigotes migrate to the intestine where they divide intensely and attach to the perimicrovillar membranes which are secreted by intestinal cells of posterior midgut [4, 5]. This adhesion step seems to be important to trigger the process of transformation of the noninfective epimastigotes into highly infective trypomastigotes (known as metacyclic trypomastigotes). The adhesion process of epimastigotes to the perimicrovillar membranes involves the participation of surface-exposed glycoconjugates. Several proteins found in the perimicrovillar membranes seem to be involved in this process [4]. Also, surface glycoinositolphospholipids (GIPLs) of the parasite have been shown to be involved in the attachment process [5]. Several saccharides are able to inhibit parasite attachment.


Review on Trypanosoma cruzi: Host Cell Interaction.

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

Life cycle of T. cruzi showing the various forms of the protozoan in the invertebrate (triatomines) and vertebrate (mammals) hosts. Figure reproduced from the Center of Control Diseases homepage.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig1: Life cycle of T. cruzi showing the various forms of the protozoan in the invertebrate (triatomines) and vertebrate (mammals) hosts. Figure reproduced from the Center of Control Diseases homepage.
Mentions: One specific feature of the trypanosomatids is that they change their general shape during their life cycle. In those species that switch from vertebrate to invertebrate hosts, this and other changes may be dramatic, involving the appearance of developmental stages which do not divide and stages which are highly infective through a process generally described as protozoan differentiation or transformation [1, 2]. Among the trypanosomatids, T. cruzi presents one of the most complex life cycles involving several developmental stages found in the vertebrate and the invertebrate hosts as well as in the bloodstream and within vertebrate host cells. Figure 1 shows a general view of the life cycle of this protozoan. Let us consider that the cycle starts with insects from the Reduviidae family sucking the blood of vertebrates infected with the trypomastigote forms which circulate in the bloodstream (known as bloodstream trypomastigotes). Once ingested, most of the trypomastigotes are lysed in the insect's stomach [3]. The surviving trypomastigotes transform, in a few days later, either into spherical stage (known as spheromastigotes) or into epimastigote stage. Epimastigotes migrate to the intestine where they divide intensely and attach to the perimicrovillar membranes which are secreted by intestinal cells of posterior midgut [4, 5]. This adhesion step seems to be important to trigger the process of transformation of the noninfective epimastigotes into highly infective trypomastigotes (known as metacyclic trypomastigotes). The adhesion process of epimastigotes to the perimicrovillar membranes involves the participation of surface-exposed glycoconjugates. Several proteins found in the perimicrovillar membranes seem to be involved in this process [4]. Also, surface glycoinositolphospholipids (GIPLs) of the parasite have been shown to be involved in the attachment process [5]. Several saccharides are able to inhibit parasite attachment.

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