Pub Date : 2019-12-18DOI: 10.5772/intechopen.84359
A. Reyes, José Luis Rosales Encina
Trypanosoma cruzi has a complex life cycle that involves a vertebrate as well as an invertebrate host. In this, last two stages are present: trypomastigotes, the flagel-lated and infective stage and the amastigote, which is the replicative stage. T. cruzi is considered one of the most successful intracellular parasites, because it cannot be eliminated by the immune system and has the capacity of invading, surviving, and replicating inside the host cells. The effects that the infection has over the immune system have been widely studied at the molecular and cellular level. However, understanding the mechanisms that the parasite uses to evade the immune system to persist in the infected individual is necessary for the effective development of drugs and/or vaccines. In this chapter, a compilation of the already described mechanisms will be carried out.
{"title":"Trypanosoma cruziInfection: Mechanisms of Evasion of Immune Response","authors":"A. Reyes, José Luis Rosales Encina","doi":"10.5772/intechopen.84359","DOIUrl":"https://doi.org/10.5772/intechopen.84359","url":null,"abstract":"Trypanosoma cruzi has a complex life cycle that involves a vertebrate as well as an invertebrate host. In this, last two stages are present: trypomastigotes, the flagel-lated and infective stage and the amastigote, which is the replicative stage. T. cruzi is considered one of the most successful intracellular parasites, because it cannot be eliminated by the immune system and has the capacity of invading, surviving, and replicating inside the host cells. The effects that the infection has over the immune system have been widely studied at the molecular and cellular level. However, understanding the mechanisms that the parasite uses to evade the immune system to persist in the infected individual is necessary for the effective development of drugs and/or vaccines. In this chapter, a compilation of the already described mechanisms will be carried out.","PeriodicalId":245699,"journal":{"name":"Biology ofTrypanosoma cruzi","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132072640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-10-04DOI: 10.5772/intechopen.84639
K. Onyekwelu
Trypanosoma cruzi ( T. cruzi ) is a protozoan parasite that causes Chagas disease, a zoonotic disease that can be transmitted to humans by blood-sucking triatomine bugs. T. cruzi is a single-celled eukaryote with a complex life cycle alternating between reduviid bug invertebrate vectors and vertebrate hosts. This article will look at the developmental stages of T. cruzi in the invertebrate vector and the vertebrate hosts, the different surface membrane proteins involved in different life cycle stages of T. cruzi , roles of different amino acids in the life cycle, carbon and energy sources and gene expression in the life cycle of T. cruzi . The author will also look at extracellular vesicles (EV) and its role in the dissemination and survival of T. cruzi in mammalian host.
{"title":"Life Cycle ofTrypanosoma cruziin the Invertebrate and the Vertebrate Hosts","authors":"K. Onyekwelu","doi":"10.5772/intechopen.84639","DOIUrl":"https://doi.org/10.5772/intechopen.84639","url":null,"abstract":"Trypanosoma cruzi ( T. cruzi ) is a protozoan parasite that causes Chagas disease, a zoonotic disease that can be transmitted to humans by blood-sucking triatomine bugs. T. cruzi is a single-celled eukaryote with a complex life cycle alternating between reduviid bug invertebrate vectors and vertebrate hosts. This article will look at the developmental stages of T. cruzi in the invertebrate vector and the vertebrate hosts, the different surface membrane proteins involved in different life cycle stages of T. cruzi , roles of different amino acids in the life cycle, carbon and energy sources and gene expression in the life cycle of T. cruzi . The author will also look at extracellular vesicles (EV) and its role in the dissemination and survival of T. cruzi in mammalian host.","PeriodicalId":245699,"journal":{"name":"Biology ofTrypanosoma cruzi","volume":"41 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129080558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-08-07DOI: 10.5772/INTECHOPEN.85010
L. Gutiérrez-Kobeh, A. Wilkins-Rodríguez
Trypanosoma cruzi is the causal agent of Chagas disease that affects 6–7 million people around the world, principally in Latin America. This disease is characterized for the presence of an acute phase in which the host immune response plays a central role in the elimination of the parasite. If the parasite is not efficiently eliminated, patients can remain asymptomatic or develop a chronic infection. One of the cells that are primarily infected with this intracellular parasite is macrophages (M ϕ ). M ϕ present a wide array of activation states with classically activated macrophages in one pole (CAM ϕ ) and alternatively activated macrophages (AAM ϕ ) in the other. One of the most important differences between these two activation states is the presence of the inducible nitric oxide synthase (iNOS or NOS2) in CAM ϕ and arginase 1 (Arg-1) in AAM ϕ ; both enzymes share the same substrate, l-arginine, and are reciprocally regulated by the action of Th1 cytokines in the case of NOS2 and Th2 cytokines in the case of Arg-1. The activation of CAM ϕ permits the production of nitric oxide (NO), highly trypanotoxic, while the activation of AAM ϕ allows the synthesis of polyamines, necessary for parasite duplication. l-arginine is a very important metabolite situated in the center between the elimination and perpetuation of T. cruzi .
{"title":"L-arginine Metabolism in the Infection withTrypanosoma cruzi","authors":"L. Gutiérrez-Kobeh, A. Wilkins-Rodríguez","doi":"10.5772/INTECHOPEN.85010","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.85010","url":null,"abstract":"Trypanosoma cruzi is the causal agent of Chagas disease that affects 6–7 million people around the world, principally in Latin America. This disease is characterized for the presence of an acute phase in which the host immune response plays a central role in the elimination of the parasite. If the parasite is not efficiently eliminated, patients can remain asymptomatic or develop a chronic infection. One of the cells that are primarily infected with this intracellular parasite is macrophages (M ϕ ). M ϕ present a wide array of activation states with classically activated macrophages in one pole (CAM ϕ ) and alternatively activated macrophages (AAM ϕ ) in the other. One of the most important differences between these two activation states is the presence of the inducible nitric oxide synthase (iNOS or NOS2) in CAM ϕ and arginase 1 (Arg-1) in AAM ϕ ; both enzymes share the same substrate, l-arginine, and are reciprocally regulated by the action of Th1 cytokines in the case of NOS2 and Th2 cytokines in the case of Arg-1. The activation of CAM ϕ permits the production of nitric oxide (NO), highly trypanotoxic, while the activation of AAM ϕ allows the synthesis of polyamines, necessary for parasite duplication. l-arginine is a very important metabolite situated in the center between the elimination and perpetuation of T. cruzi .","PeriodicalId":245699,"journal":{"name":"Biology ofTrypanosoma cruzi","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131392184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2019-06-19DOI: 10.5772/INTECHOPEN.86046
E. Barrias, L. Reignault, W. Souza
Trypanosoma cruzi , the etiological agent of Chagas disease, is an intracellular parasite that targets specific proteins of the host cell resulting in the generation of a unique parasitophorous vacuole (PV). As an intracellular parasite, T. cruzi interacts with cells from the mammalian host. Here we review aspects related with the binding of the main infective developmental stage (trypomastigote) to the host cell and its recognition by surface-exposed ligands/receptors. This process involves numerous signaling pathways and culminates in the entry of the parasite and modifications in both cells. The invasion of trypomastigotes occurs through multiple endocytic process, assembly of the PV, interaction of this vacuole with the endolysosomal system, lysis of the PV membrane, and multiplication of amastigotes within the cell in direct contact with host cell organelles.
{"title":"How Does the Main Infective Stage ofT. cruziEnter and Avoid Degradation in Host Cells? A Description of the Pathways and Organelles Involved on These Processes","authors":"E. Barrias, L. Reignault, W. Souza","doi":"10.5772/INTECHOPEN.86046","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.86046","url":null,"abstract":"Trypanosoma cruzi , the etiological agent of Chagas disease, is an intracellular parasite that targets specific proteins of the host cell resulting in the generation of a unique parasitophorous vacuole (PV). As an intracellular parasite, T. cruzi interacts with cells from the mammalian host. Here we review aspects related with the binding of the main infective developmental stage (trypomastigote) to the host cell and its recognition by surface-exposed ligands/receptors. This process involves numerous signaling pathways and culminates in the entry of the parasite and modifications in both cells. The invasion of trypomastigotes occurs through multiple endocytic process, assembly of the PV, interaction of this vacuole with the endolysosomal system, lysis of the PV membrane, and multiplication of amastigotes within the cell in direct contact with host cell organelles.","PeriodicalId":245699,"journal":{"name":"Biology ofTrypanosoma cruzi","volume":"113 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2019-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128451835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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