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Review on Trypanosoma cruzi: Host Cell Interaction  [PDF]
Wanderley de Souza,Tecia Maria Ulisses de Carvalho,Emile Santos Barrias
International Journal of Cell Biology , 2010, DOI: 10.1155/2010/295394
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. 1. Introduction to T. cruzi and Its Life Cycle Protozoa of the Trypanosomatidae family are agents of parasitic diseases that have a high incidence and a negative economic impact in developing countries. In the case of leishmaniasis, caused by several species of Leishmania, about sixteen million people are infected in Africa, Asia, parts of Europe, and Latin America. Sleeping sickness, caused by the Trypanosoma brucei group, affects about three million people in Africa. In the case of Chagas’ disease, caused by Trypanosoma cruzi, sixteen to eighteen million individuals are infected and more than 80 million are at risk of infection (http://www.who.org/). Some trypanosome species are also important in veterinary medicine, since they have been seriously affecting animals of economic interest such as horses and cattle. Diseases caused by plant trypanosomatids are increasing in importance owing to the serious problems they have caused in coconut and oil palm plantations in South America. 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
Current understanding of the Trypanosoma cruzi-cardiomyocyte interaction  [PDF]
Claudia M. Calvet,Tatiana G. Melo,Luciana R. Garzoni,Francisco O. R. Oliveira Jr.,Mirian C. S. Pereira
Frontiers in Immunology , 2012, DOI: 10.3389/fimmu.2012.00327
Abstract: Trypanosoma cruzi, the etiological agent of Chagas disease, exhibits multiple strategies to ensure its establishment and persistence in the host. Although this parasite has the ability to infect different organs, heart impairment is the most frequent clinical manifestation of the disease. Advances in knowledge of T. cruzi–cardiomyocyte interactions have contributed to a better understanding of the biological events involved in the pathogenesis of Chagas disease. This brief review focuses on the current understanding of molecules involved in T. cruzi–cardiomyocyte recognition, the mechanism of invasion, and on the effect of intracellular development of T. cruzi on the structural organization and molecular response of the target cell.
Trypanosoma cruzi: effect of phenothiazines on the parasite and its interaction with host cells
Castro, Solange L. de;Soeiro, Maria Nazaré C.;Meirelles, Maria de Nazareth Leal de;
Memórias do Instituto Oswaldo Cruz , 1992, DOI: 10.1590/S0074-02761992000200007
Abstract: phenothiazines were observed to have a direct effect on trypanosoma cruzi and on its in vitro interaction with host cells. they caused lysis of trypomastigotes (50 um/24 h) and,to a lesser extent, epimastigote proliferation. treatment of infected peritoneal macrophages with 12.5 um chlorpromazine or triflupromazine inhibited the infection; this effect was found to be partially reversible if the drugs were removed after 24 h of treatment. at 60 um, the drugs caused damage to amastigotes interiorized in heart muscle cells. however, the narrow margin of toxity between anti-trypanossomal activity and damage to host cells mitigates against in vivo investigation at the present time. possible hypothesis for the mechanism of action of phenothiazines are discussed.
Trypanosoma cruzi-cardiomyocytes: new contributions regarding a better understanding of this interaction
Meirelles, Maria de Nazareth Leal de;Pereira, Mirian Claudia S;Singer, Robert H;Soeiro, Maria de Nazaré C;Garzoni, Luciana R;Silva, Dayse T;Barbosa, Helene S;Araujo-Jorge, Tania C;Masuda, Masako O;Capella, Marcia AM;Lopes, Anibal Gil;Vermelho, Alane B;
Memórias do Instituto Oswaldo Cruz , 1999, DOI: 10.1590/S0074-02761999000700017
Abstract: the present paper summarizes new approaches regarding the progress done to the understanding of the interaction of trypanosoma cruzi-cardiomyocytes. mannose receptors localized at the surface of heart muscle cell are involved in binding and uptake of the parasite. one of the most striking events in the parasite-heart muscle cells interaction is the disruption of the actin cytoskeleton. we have investigated the regulation of the actin mrna during the cytopathology induced in myocardial cells by the parasite. t. cruzi invasion increases calcium resting levels in cardiomyocytes. we have previously shown that ca2+ atpase of the sarcoplasmic reticulum (serca) is involved in the invasion of t. cruzi in cardiomyocytes. treating the cells with thapsigargin, a drug that binds to all serca atpases and causes depletion of intracellular calcium stores, we found a 75% inhibition in the t. cruzi-cardiomyocytes invasion.
Trypanosoma cruzi-cardiomyocytes: new contributions regarding a better understanding of this interaction  [cached]
Meirelles Maria de Nazareth Leal de,Pereira Mirian Claudia S,Singer Robert H,Soeiro Maria de Nazaré C
Memórias do Instituto Oswaldo Cruz , 1999,
Abstract: The present paper summarizes new approaches regarding the progress done to the understanding of the interaction of Trypanosoma cruzi-cardiomyocytes. Mannose receptors localized at the surface of heart muscle cell are involved in binding and uptake of the parasite. One of the most striking events in the parasite-heart muscle cells interaction is the disruption of the actin cytoskeleton. We have investigated the regulation of the actin mRNA during the cytopathology induced in myocardial cells by the parasite. T. cruzi invasion increases calcium resting levels in cardiomyocytes. We have previously shown that Ca2+ ATPase of the sarcoplasmic reticulum (SERCA) is involved in the invasion of T. cruzi in cardiomyocytes. Treating the cells with thapsigargin, a drug that binds to all SERCA ATPases and causes depletion of intracellular calcium stores, we found a 75% inhibition in the T. cruzi-cardiomyocytes invasion.
Sialoglycoconjugates in Trypanosoma cruzi-host cell interaction: possible biological model - a review
Vermelho, Alane Beatriz;Meirelles, Maria Nazareth Leal;
Memórias do Instituto Oswaldo Cruz , 1994, DOI: 10.1590/S0074-02761994000100013
Abstract: a number of glycoconjugates, including glycolipids and glycoproteins, participate in the process of host-cell invasion by trypanosoma cruzi and one of the most important carbohydrates involved on this interaction is sialic acid. it is known that parasite trans-sialidase participates with sialic acid in a coordinated fashion in the initial stages of invasion. given the importance of these sialogycoconjugates, this review sets out various possible biological models for the interaction between the parasite and mammalian cells that possess a sialylated receptor/ligand system.
Interaction between Didelphis albiventris and Triatoma infestans in relation to Trypanosoma cruzi transmission
Schweigmann, Nicolás J.;Pietrokovsky, Silvia;Bottazzi, Victoria;Conti, Osvaldo;Wisnivesky-Colli, Cristina;
Memórias do Instituto Oswaldo Cruz , 1995, DOI: 10.1590/S0074-02761995000600003
Abstract: this paper attempts to prove if a high trypanosoma cruzi prevalence of opossums might be reached with few potential infective contacts. one non-infected didelphis albiventris to t. cruzi and 10 infected nymphs of triatoma infestans were left together during 23 hr in a device that simulated a natural opossum burrow. twenty-six replicates were perfomed using marsupials and triatomines only once. potentially infective contacts occurred in all the trials. from the 26 opossums used in trials, 54% did not eat any bug. of the 260 bugs used, 21% were predated. in the 25 trials involving 205 surving bugs, 36 % of them did not feed. in 15/25 cases, maior ou igual a 60% of the triatomines were able to feed. the parasitological follow-up of 24 opossums showed that among 10 that had eaten bugs, 4 turned out infected and among the 14 that had not predate, 3 (21%) became positive. in sum, 7/24 (29%) of the marsupials acquired the infection after the experiment. this infection rate was similar to the prevalences found for the opossum population of santiago del estero, argentina, suggesting that the prevalences observed in the field might be reached if each marsupial would encounter infected bugs just once in its lifetime.
Effect of drugs on Trypanosoma cruzi and on its interaction with heart muscle cell in vitro
Castro, Solange L. de;Meirelles, Maria de Nazareth L. de;
Memórias do Instituto Oswaldo Cruz , 1987, DOI: 10.1590/S0074-02761987000200009
Abstract: megazol, nifurtimox, benznidazol and allopurinol were investigated, by light and electron μscopy, for their action on t. cruzi. both the direct effect upon amastigote and trypomastigote forms and the effect upon the interaction of heart muscle cells (hmc) with bloodstream trypomastigotes were studied. the proliferation of amastigotes in warren medium was inhibited in a dose-dependent manner by megazol, nifurtimox and benznidazol. treatment of amastigotes (25-50 μm/24 h) and trypomastigotes (25 μm/24h) led to several ultrastructural alterations in the parasites. these three drugs also had a potent effect on the treatment of infected heart muscle cells when added at the beginning of the interaction or after one or three days of infection. the interiorized parasites showed a similar pattern of ultrastructural alterations as observed by the direct effect on the amastigotes. the primary heart muscle cell culture proved to be a suitable model for the study of drugs on intracellular parasites. likewise, the amastigote proliferation in axenic medium was shown to be an adequate assay for an initial trial of drugs. these parameters seem very reliable to us for a systematic investigation of the mechanism of action of new drugs.
The Interaction of Classical Complement Component C1 with Parasite and Host Calreticulin Mediates Trypanosoma cruzi Infection of Human Placenta  [PDF]
Christian Castillo,Galia Ramírez,Carolina Valck,Lorena Aguilar,Ismael Maldonado,Carlos Rosas,Norbel Galanti,Ulrike Kemmerling ,Arturo Ferreira
PLOS Neglected Tropical Diseases , 2013, DOI: 10.1371/journal.pntd.0002376
Abstract: Background 9 million people are infected with Trypanosoma cruzi in Latin America, plus more than 300,000 in the United States, Canada, Europe, Australia, and Japan. Approximately 30% of infected individuals develop circulatory or digestive pathology. While in underdeveloped countries transmission is mainly through hematophagous arthropods, transplacental infection prevails in developed ones. Methodology/Principal Findings During infection, T. cruzi calreticulin (TcCRT) translocates from the endoplasmic reticulum to the area of flagellum emergence. There, TcCRT acts as virulence factor since it binds maternal classical complement component C1q that recognizes human calreticulin (HuCRT) in placenta, with increased parasite infectivity. As measured ex vivo by quantitative PCR in human placenta chorionic villi explants (HPCVE) (the closest available correlate of human congenital T. cruzi infection), C1q mediated up to a 3–5-fold increase in parasite load. Because anti-TcCRT and anti-HuCRT F(ab′)2 antibody fragments are devoid of their Fc-dependent capacity to recruit C1q, they reverted the C1q-mediated increase in parasite load by respectively preventing its interaction with cell-bound CRTs from both parasite and HPCVE origins. The use of competing fluid-phase recombinant HuCRT and F(ab′)2 antibody fragments anti-TcCRT corroborated this. These results are consistent with a high expression of fetal CRT on placental free chorionic villi. Increased C1q-mediated infection is paralleled by placental tissue damage, as evidenced by histopathology, a damage that is ameliorated by anti-TcCRT F(ab′)2 antibody fragments or fluid-phase HuCRT. Conclusions/Significance T. cruzi infection of HPCVE is importantly mediated by human and parasite CRTs and C1q. Most likely, C1q bridges CRT on the parasite surface with its receptor orthologue on human placental cells, thus facilitating the first encounter between the parasite and the fetal derived placental tissue. The results presented here have several potential translational medicine aspects, specifically related with the capacity of antibody fragments to inhibit the C1q/CRT interactions and thus T. cruzi infectivity.
F(ab')2 antibody fragments against Trypanosoma cruzi calreticulin inhibit its interaction with the first component of human complement
Biological Research , 2005, DOI: 10.4067/S0716-97602005000200008
Abstract: trypanosoma cruzi calreticulin (tccrt), described in our laboratory, retains several important functional features from its vertebrate homologues. we have shown that recombinant tccrt inhibits the human complement system when it binds to the collagenous portion of c1q. the generation of classical pathway convertases and membrane attack complexes is thus strongly inhibited. in most t. cruzi-infected individuals, tccrt is immunogenic and mediates the generation of specific antibodies. by reverting the c1q / tccrt interaction, a parasite immune evasion strategy, these antibodies contribute to the host / parasite equilibrium. in an in vitro correlate of this situation, we show that the c1q / tccrt interaction is inhibited by f(ab')2 polyclonal anti-tccrt igg fragments. it is therefore feasible that in infected humans anti-tccrt antibodies participate in reverting an important parasite strategy aimed at inhibiting the classical complement pathway. thus, membrane-bound tccrt interacts with the collagenous portion c1q, and this c1q is recognized by the cd91-bound host cell crt, thus facilitating parasite internalization. based on our in vitro results, it could be proposed that the in vivo interaction between tccrt and vertebrate c1q could be inhibited by f(ab')2 fragments anti-rtccrt or against its s functional domain, thus interfering with the internalization process
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