Дисертації з теми "Metabolism in Toxoplasma Gondii"
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Roohi, Aysha. "Toxoplasma gondii infection and the host cell metabolism." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648369.
Повний текст джерелаRen, Bingjian. "Physiological importance of phospholipid biogenesis in Toxoplasma gondii." Doctoral thesis, Humboldt-Universität zu Berlin, 2019. http://dx.doi.org/10.18452/20721.
Повний текст джерелаToxoplasma gondii is an obligate intracellular parasite that causes Toxoplasmosis in human and livestock. Phospholipid biosynthesis is crucial for the successful intracellular survival and replication of the parasites, as the phospholipids have important roles in the biogenesis of membrane organelles, signal transduction and other cellular processes. Here, we dissected the physiological importance of two pathways accounting for the synthesis of PtdEtn and PtdIns. We demonstrated the presence of a novel PtdIns synthase (PIS) in T.gondii termed TgPIS, expressing a functional enzyme with a catalytically vital CDP-alcohol phosphotransferase motif, which resides exclusively in the Golgi body. The parasite imports myo-inositol from milieu, and co-utilizes de novo-synthesized CDP-diacylglycerol to produce PtdIns. An auxin-inducible conditional repression of TgPIS abrogated the lytic cycle of the parasite in mammalian cells due to defects in the replication, motility and egress. Lipidomic profiling of the PIS mutant demonstrated selective reduction of certain PtdIns and PtdThr species, whereas selected PtdGro, PtdSer and BMP species were increased, which suggested a tight inter-regulation and homeostasis of anionic phospholipids to maintain the membrane integrity. In addition, we identified an ethanolamine cytidyltransferase (TgECT), the rate-limiting enzyme of Kennedy pathway, which is localized in the cytosol. The enzyme is clearly essential for the lytic cycle as its genetic ablation was not feasible, and auxin-meditated conditional knockdown severely impaired the parasite growth in plaque assays. Similarly, lipidomic analysis of the mutant identified an important role in the biogenesis of selected species of PtdEtn, PtdSer and PtdThr. Moreover, we discovered that TgECT is required for the generation of ethanolamine-phosphory ceramide (EPC), a rare sphingolipid present only a limited number of organisms.
Nitzsche, Richard. "Genetic dissection of the central carbon metabolism in the intracellular parasite Toxoplasma gondii." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2017. http://dx.doi.org/10.18452/17744.
Повний текст джерелаToxoplasma gondii is a widespread protozoan parasite, infecting nearly all warm-blooded organisms. Asexual reproduction of the parasite within its host cells is achieved by consecutive lytic cycles, which necessitates biogenesis of significant energy and biomass. This work shows that glucose and glutamine are the two major physiologically important nutrients used for the synthesis of macromolecules (ATP, nucleic acid, proteins and lipids) in T. gondii, and either of them is sufficient to ensure the parasite survival. The parasite can counteract genetic ablation of its glucose transporter by increasing the flux of glutamine-derived carbon through the TCA cycle and by concurrently activating gluconeogenesis, which guarantee a continued biogenesis of ATP and biomass for host-cell invasion and parasite replication, respectively. Growth defect in the glycolysis-impaired mutant is caused by a compromised synthesis of lipids, which cannot be counterbalanced by glutamine, but can be restored by acetate. Consistently, supplementation of parasite cultures with exogenous acetate can amend the lytic cycle of the glucose transport mutant. Furthermore, this work revealed two discrete phosphoenolpyruvate carboxykinase (PEPCK) enzymes in the parasite, one of which resides in the mitochondrion (TgPEPCKmt), whereas the other protein is not expressed in tachyzoites (TgPEPCKnet). Parasites with an intact glycolysis can tolerate genetic deletions of TgPEPCKmt as well as of TgPEPCKnet, indicating their nonessential roles for the tachyzoite survival. TgPEPCKnet can also be ablated in glycolysis-deficient mutant, whereas TgPEPCKmt is refractory to deletion. In accord, the lytic cycle of a conditional mutant of TgPEPCKmt in the glycolysis-impaired strain was aborted upon induced repression of the mitochondrial isoform, demonstrating its essential role for the glucose-independent survival of tachyzoites.
Sampels, Vera. "Plasticity of the phosphatidylcholine biogenesis in the obligate intracellular Parasite Toxoplasma gondii." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16491.
Повний текст джерелаToxoplasma gondii is an obligate intracellular apicomplexan parasite that causes life-threatening disease in neonates and in immunocompromised people. Successful replication of Toxoplasma requires substantial membrane biogenesis, which must be satisfied irrespective of the host-cell milieu. Like in other eukaryotes, the two most abundant phospholipids in the T. gondii membrane are phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn). Bioinformatics and precursor labeling analyses confirm their synthesis via the CDP-choline and CDP-ethanolamine pathway, respectively. This work shows that the 3-step CDP-choline pathway, involving the activities of TgCK, TgCCT and TgCPT, localizes to the cytosol, nucleus and ER membrane, respectively. The initial reaction is catalyzed by a dual-specificity choline kinase (TgCK, ~70-kDa), capable of phosphorylating choline as well as ethanolamine. The purified full-length TgCK displayed a low affinity for choline (Km ~0.77 mM). TgCK harbors a unique N-terminal hydrophobic peptide that is required for the formation of enzyme oligomers in the parasite cytosol but not for activity. The displacement of the TgCK promoter in a conditional mutant of T. gondii (deltatgcki) attenuated the enzyme expression by ~80%. Unexpectedly, the ?tgcki mutant was not impaired in intracellular growth, and exhibited a normal PtdCho biogenesis. To recompense for the loss of full-length TgCK, the mutant appears to make use of an alternative promoter and/or start codon, resulting in the expression of a shorter but active TgCK isoform identified by the anti-TgCK antiserum, which correlated with its persistent choline kinase activity. Accordingly, the ?tgcki showed an expected incorporation of choline into PtdCho, and susceptibility to dimethylethanolamine (a choline analog). Interestingly, the conditional mutant displayed a regular growth in off state despite a 25% decline in PtdCho content, which suggests a compositional flexibility in T. gondii membranes and insignificant salvage of host-derived PtdCho. The two-step conditional mutagenesis of TgCCT, which caused a reduced growth rate to about 50%, further substantiated this finding. The enzymatic activity of TgCCT and its role in PtdCho synthesis remain to be proven, however. Taken together, the results demonstrate that the CDP-route is likely essential in T. gondii. The competitive inhibition of choline kinase to block the parasite replication appears a potential therapeutic application.The work also reveals a remarkably adaptable membrane biogenesis in T. gondii, which may underly the evolution of Toxoplasma as a promiscuous pathogen.
Sundaram, Lalitha Sridevi. "Toxoplasma gondii-mediated host cell transcriptional changes lead to metabolic alterations akin to the Warburg effect." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/267958.
Повний текст джерелаBlume, Martin. "Characterization of the differential significance of sugar Import in the apicomplexan parasites Toxoplasma gondii and Plasmodium." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2011. http://dx.doi.org/10.18452/16396.
Повний текст джерелаToxoplasma gondii and Plasmodium species are obligate intracellular pathogens that utilize host sugars for energy homeostasis and macro molecular synthesis. Here, we report that the T. gondii glucose transporter, TgGT1, and of its homologs of P. falciparum and P. berghei (PfHT1 and PbHT1) transport glucose, mannose, galactose and fructose. Besides TgGT1, Toxoplasma harbours one additional surface localized putative sugar transporter (TgST2). Surprisingly both Proteins are nonessential and only the deletion of TgGT1 inflicts a mild defect in the parasite replication. The ?tggt1 mutant is unable to import glucose and consequently displays an attenuated glucose-dependent motility, which is completely rescued by glutamine. ?tggt1 performs increased glutamine metabolism that is sufficient to sustain motility and replication. The ?tggt1 strain provides a model for further investigating its adaptation to disparate host cells. In contrast to T. gondii, erythrocytic stages of Plasmodium species critically depend on glucose uptake, and the PfHT1 transporter is considered as a drug target against human malaria. Here, we report that PbHT1 (a PfHT1 homolog) is also essential for blood stage development in the rodent malaria parasite P. berghei. PbHT1 is expressed throughout the life cycle. Moreover, a PfHT1- and PbHT1-specific sugar analogue, compound 3361, can inhibit the hepatic development and ookinete formation in P. berghei. These results signify that PbHT1 and exogenous glucose are also required during the ex-erythrocytic stages of P. berghei. To permit a high-throughput screening of selective PfHT1 inhibitors and their subsequent in vivo assessment, we have established a PfHT1-expressing Saccharomyces cerevisiae mutant and generated a PfHT1-dependent ?pbht1 of P. berghei strain. This thesis underscores various previously unknown aspects of sugar metabolism in Toxoplasma and Plasmodium, and unravel their metabolic differences.
Molan, Aus. "Involvement of Toxoplasma gondii and associated inflammatory markers in the pathogenesis of type 2 diabetes mellitus." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2020. https://ro.ecu.edu.au/theses/2338.
Повний текст джерелаCosta, Beatriz Guerreiro Basilio. "Estudo da modulação do metabolismo lipídico de células dendríticas humanas na infecção por Toxoplasma gondii." Instituto Oswaldo Cruz, 2012. https://www.arca.fiocruz.br/handle/icict/7036.
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Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ, Brasil
A toxoplasmose é uma doença de alta prevalência no mundo, causada pelo Toxoplasma gondii, um parasita intracelular obrigatório. O T. gondii possui mecanismos de modulação do metabolismo do seu hospedeiro que garantem sua sobrevivência e a instalação da infecção crônica. Um dos tipos celulares mais permissivos à infecção e multiplicação do T. gondii são as células dendríticas (DC), paradoxalmente as células apresentadoras de antígeno mais eficazes, com capacidade de deflagrar uma resposta imune protetora eficaz e duradoura. Neste trabalho, estudamos a modulação do metabolismo lipídico de células dendríticas humanas na infecção por T. gondii. Mostramos que o parasita induziu a maturação da célula e um padrão misto de resposta inflamatória, com altas concentrações das citocinas pró-inflamatórias IL-6 e TNF- e da citocina antiinflamatória IL-10. Após 3 horas de infecção, verificamos que T. gondii induziu a expressão gênica de ciclooxigenase-2 (COX-2). De forma importante, observamos por qRT-PCR que a infecção com T. gondii regulou positivamente a expressão do gene do receptor nuclear (RN) regulado por lipídios PPAR, mas não do LXR. Já a expressão do mRNA das moléculas envolvidas no transporte e estoque de lipídios, FABP4 e ADRP, alvos do PPAR, e ABCA1, alvo do LXR, foram aumentadas pela infecção de 3 horas com o parasita. Utilizando duas técnicas distintas (BODIPY e coloração com ósmio) avaliamos a biogênese de corpúsculos lipídicos (CL) após infecção com o T. gondii e constatamos que essas organelas não foram induzidas após 3 horas de infecção. Entretanto, após 24 horas, 90% das DC apresentaram CL e o número de CL por DC foi estatisticamente maior. Observamos a presença de CL em DC não infectadas pelo parasita, mostrando que a indução da biogênese de CL é um fenômeno parácrino, não dependente da infecção celular. Avaliamos também a importância do PPAR na infecção por T. gondii, através do tratamento das DC com seu agonista ou antagonista. Após 3 horas, apenas os genes ADRP, FABP4 e ABCA1, alvos dos receptores nucleares, foram modulados. Por último, investigamos a influência do T. gondii na expressão das moléculas apresentadoras de antígenos lipídicos. Por citometria de fluxo, constatamos que não há alteração na expressão de membrana dessas moléculas. Contudo, por qRT-PCR, observamos que o T. gondii regula negativamente a expressão dos genes cd1d e cd1e. Em conclusão, mostramos que T. gondii foi capaz de regular positivamente o metabolismo lipídico das DC e negativamente as moléculas apresentadoras de lipídios CD1, sem a participação essencial de PPAR nesses processos.
Toxoplasmosis is a worldwide high prevalence disease caused by Toxoplasma gondii, an obligate intracellular parasite. T. gondii developed mechanisms for modulating the metabolism of its host, ensuring their survival and the chronic infection. Dendritic cells (DC) are one of the most permissive cell types to T. gondii infection and replication and are, paradoxically, considered the most effective antigen presenting cells, triggering an effective and long-lasting protective immune response. In this work, we studied the modulation of lipid metabolism in human dendritic cells infected with T. gondii. We showed that the parasite induced cell maturation, and a mixed pattern of inflammatory response with high levels of proinflammatory cytokines IL-6 and TNF-, and anti-inflammatory cytokine IL-10. After 3h of infection, we found that T. gondii induced increased gene expression of cyclooxygenase-2 (COX-2). Importantly, we observed by qRT-PCR that T. gondii infection upregulated the nuclear receptor (RN) PPAR gene expression, while the levels of LXR were unchanged. Furthermore, the mRNA expression of molecules involved in the transport and storage of lipids, FABP4 and ADRP, PPARtargets, and ABCA1, LXR target, were also increased at 3h of infection with the parasite. In parallel, using two different techniques, (BODIPY and osmium staining), we evaluated the biogenesis of lipid droplets (LD) after infection with T. gondii, and observed that these organelles were not induced after 3 hours of infection. However, after 24 hours, 90% of DC showed LD and the number of LD per DC was statistically enhanced. We observed the presence of LD in DC not infected with the parasite, showing that induction of biogenesis of LD is a paracrine phenomenon not dependent on cell infection. We also evaluated the role of PPAR in T. gondii infection by treating DC with its agonist or antagonist. After 3 hours of infection only the nuclear receptor target genes ADRP, FABP4 and ABCA1 were modulated. Finally, we investigated the influence of T. gondii in the expression of lipid antigens presenting molecules. By flow cytometry, we observed no variation in expression of these molecules in cell membrane. However, by qRT-PCR, we found that the T. gondii downregulated gene expression of cd1d and cd1e. In conclusion, we showed that T. gondii was able to upregulate the DC lipid metabolism, and downregulate CD1 lipid presentation. Apparently, the RN PPAR has no essential role in this process.
Silva, Camila Luna da. "Estudo do metabolismo mitocondrial e da resposta anti-apoptótica de células endoteliais humanas durante a evolução da infecção por taquizoítos de Toxoplasma gondii." Universidade do Estado do Rio de Janeiro, 2013. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=8172.
Повний текст джерелаA toxoplasmose é uma zoonose amplamente distribuída que afeta mais de um terço da população mundial e de grande importância na saúde pública. A maioria das infecções em humanos por Toxoplasma gondii é assintomática. A toxoplasmose é amplamente investigada visto que se apresenta como uma doença grave em pessoas imunodeprimidas (portadores da síndrome da imunodeficiência adquirida (SIDA), não tratados, indivíduos transplantados, paciente em tratamento quimioterápico ou em uso de drogas supressoras e gestantes). A toxoplasmose congênita frequentemente pode levar ao aborto espontâneo ou até mesmo resultar na formação de crianças com algum grau de atraso no desenvolvimento mental e/ou físicos, deste modo, a transmissão congênita pode ser muito mais importante do que se pensava, pois os parasitos encontrados na circulação sanguinea são capazes de infectar as células endoteliais dos vasos e os tecidos circunjacentes, podendo resultar no encistamento do T. gondii. Atualmente a toxoplasmose vem sendo investigada devido a sua associação a inúmeras outras doenças, assim, estudos sobre a evolução da infecção por T. gondii em diferentes tipos de células hospedeiras se fazem necessários para uma abordagem terapêutica adequada. Ao invadir a célula hospedeira o parasito possui a capacidade de recrutar as mitocôndrias promovendo mudanças na organização mitocondrial ao longo da progressão da infecção, garantindo um ambiente favorável a sua multiplicação. Diante disso, investigamos se o parasito possui a capacidade de interferir no metabolismo mitocondrial e na resposta apoptótica da célula endotelial. O presente trabalho teve como objetivo analisar o metabolismo mitocondrial através da respirometria de alta-resolução e da resposta apoptótica através do western blotting das células endoteliais da veia umbilical humana (HUVEC) infectadas por 2, 6 e 20 horas por taquizoítos de T. gondii. A respirometria de alta-resolução revelou que o parasito interfere no metabolismo energético da célula hospedeira. A análise do conteúdo de proteínas da família Bcl-2 por western blotting revelou maior estímulo apoptótico no tempo inicial de infecção, quando comparado aos demais tempos. Os resultados dos conteúdos de caspase 3, proteína efetora da apoptose, não demonstrou diferença nos tempos iniciais de infecção Entretanto, em tempos mais tardios, o conteúdo de caspase 3 mostrou-se significativamente aumentado quando comparado às HUVEC não infectadas. A dinâmica de replicação do parasito foi observada através do monitoramento pelo sistema Time-Lapse Nikon BioStation IMQ em tempo real das células infectadas por T.gondii. Portanto, nossos resultados sugerem que o protozoário ao recrutar as mitocôndrias da célula hospedeira interfere no metabolismo mitocondrial e na modulação da apoptose para garantir um ambiente favorável a sua multiplicação.
Toxoplasmosis is a widespread zoonosis that affects more than a third of the world population and of great public health importance. Most human infections with Toxoplasma gondii are asymptomatic. Toxoplasmosis is widely investigated since it presents itself as a serious disease in immunocompromised persons (holders of acquired immunodeficiency syndrome (AIDS), untreated, transplant recipients, patients undergoing chemotherapy or suppressing drugs and pregnant). Congenital toxoplasmosis can often lead to miscarriage or even result in the formation of children with some degree of developmental delay mental and / or physical, thus congenital transmission may be much more important than previously thought, because the parasites found In the bloodstream are able to infect endothelial cells of blood vessels and surrounding tissues, which may result in encystment T. gondii. Currently toxoplasmosis has been investigated because of their association with other diseases, so, studies of the evolution of T.gondii infection in different types of host cells are necessary for an adequate therapeutic approach. To invade the host cell, the parasite has the ability to recruit mitochondria promoting changes in mitochondrial organization along the progression of infection, ensuring a favorable environment for their multiplication. Therefore, we investigated whether the parasite has the ability to interfere with mitochondrial metabolism and apoptotic response of endothelial cells. This study aimed to analyze the mitochondrial metabolism by high-resolution respirometry and apoptotic response by western blotting of endothelial cells of human umbilical vein (HUVEC) infected for 2, 6 and 20 hours per tachyzoites of T. gondii. The high-resolution respirometry revealed that the parasite interferes with the energy metabolism of the host cell. The analysis of the family protein content of Bcl-2 by western blotting revealed higher apoptotic stimulus at the initial time of infection, as compared to other times. The results of the contents of caspase 3 protein effector of apoptosis, showed no difference in the initial days of infection However, in more recent times, the content of caspase 3 was significantly increased when compared to non-infected HUVEC. The dynamics of parasite replication was observed by monitoring the system Time-Lapse Nikon BioStation IMQ in real time from infected cells by T. gondii. Therefore, our findings suggest that mitochondria in recruiting protozoan host cell interfere with mitochondrial metabolism and in the modulation of apoptosis to ensure a favorable environment for multiplication.
HIRAMOTO, ROBERTO M. "Efeitos da radiacao ionizante sobre a estrutura, metabolismo e infecciosidade de um protozoario patogenico, Toxoplasma gondii (Nicolle and Manceaux, 1908)." reponame:Repositório Institucional do IPEN, 1998. http://repositorio.ipen.br:8080/xmlui/handle/123456789/10660.
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Dissertacao (Mestrado)
IPEN/D
Instituto de Pesquisas Energeticas e Nucleares - IPEN/CNEN-SP
Nitzsche, Richard [Verfasser], Nishith [Gutachter] Gupta, Kai [Gutachter] Matuschewski, and Maik [Gutachter] Lehmann. "Genetic dissection of the central carbon metabolism in the intracellular parasite Toxoplasma gondii / Richard Nitzsche ; Gutachter: Nishith Gupta, Kai Matuschewski, Maik Lehmann." Berlin : Lebenswissenschaftliche Fakultät, 2017. http://d-nb.info/1130217469/34.
Повний текст джерелаMason, Sam. "Toxoplasma gondii in sheep." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.556024.
Повний текст джерелаPaugam, André. "Protéasome de "Toxoplasma gondii"." Paris 5, 2002. http://www.theses.fr/2002PA05P611.
Повний текст джерелаXia, Dong. "Proteomics of Toxoplasma gondii." Thesis, University of Liverpool, 2009. http://livrepository.liverpool.ac.uk/1276/.
Повний текст джерелаRoch-Deries, Florance Candolfi Ermanno. "Choriorétinite à toxoplasma gondii." [S.l] : [s.n.], 2003. http://www.scd.uhp-nancy.fr/docnum/SCDMED_T_2003_ROCH_DERIES_FLORENCE.pdf.
Повний текст джерелаcom, Nevi Parameswaran@gmail, and Nivethitha (Nevi) Parameswaran. "Toxoplasma gondii in Australian Marsupials." Murdoch University, 2008. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20100203.145857.
Повний текст джерелаKremer, Katrin. "Vesicular trafficking in Toxoplasma gondii." Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4753/.
Повний текст джерелаBhalla, Mayank. "Molecular studies on Toxoplasma gondii." Thesis, University of Reading, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339977.
Повний текст джерелаParameswaran, Nevi. "Toxoplasma gondii in Australian marsupials /." Murdoch University Digital Theses Program, 2008. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20100203.145857.
Повний текст джерелаParameswaran, Nivethitha (Nevi). "Toxoplasma gondii in Australian Marsupials." Thesis, Parameswaran, Nivethitha (Nevi) (2008) Toxoplasma gondii in Australian Marsupials. PhD thesis, Murdoch University, 2008. https://researchrepository.murdoch.edu.au/id/eprint/1680/.
Повний текст джерелаParameswaran, Nivethitha (Nevi). "Toxoplasma gondii in Australian Marsupials." Parameswaran, Nivethitha (Nevi) (2008) Toxoplasma gondii in Australian Marsupials. PhD thesis, Murdoch University, 2008. http://researchrepository.murdoch.edu.au/1680/.
Повний текст джерелаChaichan, Patcharee. "Epidemiology of Toxoplasma gondii in Thailand." Thesis, Limoges, 2017. http://www.theses.fr/2017LIMO0014/document.
Повний текст джерелаToxoplasma gondii is an obligate intracellular parasite. Toxoplasma gondii infection is widespread throughout the world. Nevertheless, it is poorly studied in Southeast Asian countries including Thailand. We carried out 3 field works in Thailand to try to understand the circulation of T. gondii through a seroprevalence study in chickens in rural areas and strain isolation attempts in animals. During the two first field works, performed in Kanchanaburi province, we determined the seroprevalence in chickens (Gallus domesticus) using 2 serological tests, a Modified-Agglutination-Test (MAT) and an immunofluorescence assay (IFAT) and subsequently tried to isolate the strains of T. gondii from seropositive animals. During the third field work carried out in 3 other Thai provinces (Nakhonratchasima,Lopburi and Saraburi), we attempted to isolate strains directly from chicken carcasses sold in different markets or other dead animals.The overall seroprevalence for 600 chickens sampled over the two field works in Kanchanaburi was 17.7% (95%CI: 14.6% -20.7) and 33.0% (95% CI: 29.2-36.8), by MAT, and IFAT, respectively. The κ coefficient indicated an absence of concordance between the 2 serological tests.A total of 162 isolation attempts were performed by mouse bioassays, but no viable strain of T. gondii was isolated during these 3 field works. However, a qPCR targeting 529 bp T. gondii gene was positive for 13 digestion pellets of organs of chickens, pigeon, quail and in brains or hearts of mice inoculated with 16 other chickens. These qPCR were weaklly positive (Ct ≥33) indicating a low amount of parasite DNA in our samples that did not allow genotyping T. gondii with microsatellite markers.This work demonstrated the importance and difficulties of field work for the seroprevalence study as well as strain isolation. The isolation of T. gondii strains required intensive and complex sampling in the tropical and humid environment of Thailand. The diverse factors that could have a negative impact on our results are discussed. They might explain the absence of strain isolation from seropositive animals
Woods, Stuart. "Immunological control of toxoplasma gondii infection." Thesis, University of Strathclyde, 2012. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=19276.
Повний текст джерелаCirelli, Kimberly M. "Rodent inflammasome activation by Toxoplasma gondii." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/105635.
Повний текст джерелаCataloged from PDF version of thesis.
Includes bibliographical references.
Toxoplasma gondii is an obligate intracellular pathogen capable of chronically infecting nearly all warm-blooded animals, including humans. The chronic stage is characterized by the presence of semi-dormant cysts in brain and muscle tissues. These cysts are crucial in the success of Toxoplasma as they are orally infectious and allow for the transmission of the parasite between hosts. As the host immune response drives cyst formation, the establishment of this chronic infection relies on the parasite's ability to find a balance between activation of a host immune response and evasion of parasiticidal mechanisms. This balance is achieved through the modulation of host cell processes by parasite proteins secreted from specialized secretory organelles known as rhoptries and dense granules. Here, we report that Toxoplasma activates the inflammasomes in mice and rats. The inflammasomes are a set of cytoplasmic pattern recognition receptors (PRRs). Activation of the inflammasomes results in caspase-1 activation and the cleavage and release of the pro-inflammatory cytokines, Interleukin (IL)-1[beta] and IL-18. IL-1p is an important mediator of local inflammation and neutrophil recruitment. IL- 18 induces Interferon (IFN)-[gamma], which is a critical cytokine in the control of Toxoplasma. A form of cell death, termed pyroptosis, can accompany inflammasome activation. The NLRP3 inflammasome is activated in mouse macrophages, leading to the secretion of IL-1[beta] in vitro. The NLRP1 and NLRP3 inflammasomes play a major role in mouse survival and control of parasite replication in vivo. The NLRPI inflammasome is activated in infected macrophages from rats that are able to completely clear infection. Toxoplasma infection leads to the secretion of active IL-I[beta] and IL-18. Activation of the NLRP1 inflammasome leads to pyroptosis, a programmed form of cell death. Pyroptosis prevents parasite replication within the host cell and likely promotes clearance by nearby immune cells. Using a chemical mutagenesis screen, we identified three Toxoplasma dense granule proteins (GRAs), GRA18, GRA27 and GRA28, essential for NLRP1 inflammasome activation and pyroptosis in rat macrophages. Our work has identified Toxoplasma gondii as a novel activator of the rodent inflammasomes and demonstrated host cell death as a mechanism to control parasite replication. We have also identified three novel parasite proteins required for this activation, providing insight into interactions between parasite and host, which may aid in the treatment of human infection.
by Kimberly M. Cirelli.
Ph. D.
Ravindran, Sandeep. "Effector protein secretion by toxoplasma gondii /." May be available electronically:, 2009. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.
Повний текст джерелаBrennan, Anthea. "Toxoplasma gondii infection in Australian felines." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/15060.
Повний текст джерелаBurrells, Alison Clair. "Toxoplasma gondii in animal and human hosts." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9628.
Повний текст джерелаRiahi, Dehkordi Hamayoun. "Hammondia hammondi : études comparatives avec Toxoplasma gondii." Limoges, 1997. http://www.theses.fr/1997LIMO105E.
Повний текст джерелаLiu, Elizabeth. "The Autophagy Pathway and Toxoplasma gondii Infection." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1428103561.
Повний текст джерелаBertin, Brigitte. "Etude immunochimique des antigènes de Toxoplasma gondii." Bordeaux 2, 1985. http://www.theses.fr/1985BOR22001.
Повний текст джерелаHartmann, Jan. "Golgi and centrosome cycles in Toxoplasma gondii." [S.l. : s.n.], 2005.
Знайти повний текст джерелаBertin, Brigitte. "Etude immunochimique des antigènes de Toxoplasma gondii." Grenoble : ANRT, 1985. http://catalogue.bnf.fr/ark:/12148/cb37594507t.
Повний текст джерелаJesus, Rogerio Fernando de. "Infeccção natural por Toxoplasma gondii em quirópteros." Universidade Federal da Bahia, 2015. http://repositorio.ufba.br/ri/handle/ri/20375.
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CONS NAC DE DESENVOLVIMENTO CIENTIFICO E TECNOLOGICO - CAPES
Toxoplasma gondii é um protozoário coccídeo formador de cistos teciduais, que tem como hospedeiros definitivos os felídeos, e como hospedeiros intermediários mamíferos e aves. É um parasito disseminado em todos os continentes, que infecta aproximadamente um terço da população humana e pode causar encefalite fatal em pacientes imunodeficientes. Nos animais, tem relevância principalmente em pequenos ruminantes, por causar abortos e outras alterações reprodutivas. Quirópteros podem se infectar com T. gondii e atuarem como fonte de infecção para animais silvestres, domésticos e o homem. No Brasil, ocorre uma alta variabilidade genética do parasito, que pode ser explicada pela grande variedade de hospedeiros no ambiente silvestre. Objetivou-se com este estudo determinar a frequência de infecção em quirópteros de vida livre no estado da Bahia por T. gondii e realizar o isolamento in vivo do protozoário a partir desses animais. Foram utilizadas 124 amostras, provenientes de 97 indivíduos de sete espécies de morcegos, capturados entre os anos de 2008 e 2015, sendo encontrados dois indivíduos positivos por meio da PCR de tecidos, correspondendo a 2,06% de positividade. Nenhum isolamento foi realizado uma vez que os tecidos disponíveis para bioensaio apresentaram-se negativos na PCR
Toxoplasma gondii is a cyst-forming protozoan coccidia, which has felids as definitive hosts, and mammals and birds as intermediate hosts. It’s distributed in all continents and infects about a third of the human population. T. gondii can cause fatal encephalitis in immunodeficient patients. In animals, it’s relevant mainly in small ruminants, for causing abortions and other reproductive abnormalities. Bats can become infected with T. gondii and act as a source of infection for wild and domestic animals and man. In Brazil, there is a high genetic variability of the parasite, which can be explained by the great variety of hosts in the wild environment. The objective of this study was to determine the frequency of free-living bats infection in Bahia by T. gondii and perform in vivo isolation of the parasite from these animals. A total of 124 samples were used from 97 individuals of seven species of bats, caught between the years 2008 and 2015. Two animals were positive by tissue PCR, corresponding to 2.06% of positivity. No isolation was achieved once the tissue available for bioassay showed to be negative by PCR.
Carey, Robert Francis IV. "Toxoplasma gondii and behavioral modification in hosts." Thesis, Boston University, 2013. https://hdl.handle.net/2144/12065.
Повний текст джерелаToxoplasma gondii is a heteroxenous protozoan parasite that is found in nearly every species of mammal and billions of latently infected humans worldwide. The symptoms and morbidities associated with acute, congenital, and AIDS-associated toxoplasmosis are familiar to many, while those associated with latent toxoplasmosis are not nearly as well known. Behavioral manipulation is a common strategy of parasite and parasitoid species, and recent research into T. gondii has revealed that T. gondii infection alters the way rodents respond to the odor of the urine of its feline predators, which are also the definitive hosts of T. gondii. Humans have been found to be potentially affected by T. gondii as well: associations have been identified between latent T. gondii infection and psychiatric diseases (including schizophrenia), personality changes, and traffic accidents. This review investigates the state of current scientific knowledge related to Toxoplasma gondii, analyzes recent developments, and examines the implications on public health. We also provide critical analysis of the published literature and make suggestions for future research.
Parigi, Maria <1984>. "Toxoplasma gondii in animals and the environment." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6423/1/Parigi_Maria_tesi.pdf.
Повний текст джерелаParigi, Maria <1984>. "Toxoplasma gondii in animals and the environment." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2014. http://amsdottorato.unibo.it/6423/.
Повний текст джерелаNolan, Kay. "The transmission dynamics of Toxoplasma gondii in sheep." Thesis, University of Warwick, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479313.
Повний текст джерелаMohammed, Saleem. "Molecular studies on the protozoan parasite Toxoplasma gondii." Thesis, University of Reading, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262211.
Повний текст джерелаWheeler, Ruth Belinda. "Studies of the molecular biology of Toxoplasma gondii." Thesis, University of Reading, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356985.
Повний текст джерелаNickdel, Mohammad Barat. "Role of Th2 cytokines in Toxoplasma gondii infection." Thesis, University of Strathclyde, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248258.
Повний текст джерелаHenriquez, Fiona Luisa. "Recharacterization of Toxoplasma gondii dense granule protein GRA3." Thesis, University of Strathclyde, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.273437.
Повний текст джерелаWansadhipathi-Kannangra, Nilu Kumari. "Sphingolipid synthases of Toxoplasma gondii and other organisms." Thesis, Durham University, 2011. http://etheses.dur.ac.uk/3204/.
Повний текст джерелаGhérardi, Arnaud. "Toxoplasma gondii : étude de la purine nucléoside phosphorylase." Lyon 1, 2001. http://www.theses.fr/2001LYO1T208.
Повний текст джерелаLiew, Lloyd. "Structural studies on microneme proteins from Toxoplasma gondii." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11654.
Повний текст джерелаBouleau, Anne Pascaline. "Identification et caractérisation de métalloprotéases de Toxoplasma gondii." Thesis, Reims, 2014. http://www.theses.fr/2014REIMM202/document.
Повний текст джерелаToxoplasma gondii is an intracellular protozoan parasite which belongs to the Apicomplexa phylum. In protozoans, proteases have key roles in the parasitic cycle. They thereby are considered as virulence factors. In T. gondii, metallopeptidases may be involved in the crossing of biological barriers. Currently, only five metallopeptidases from T. gondii are described: an aminopeptidase N, two toxolysins, one leucine aminopeptidase and one FtsH1 peptidase. During the study of the influence of human monocytes invasion by T. gondii on the monocytic matrix metalloproteases expression profile, we brought out a parasitic protease showing gelatino- and elastinolytic properties.The aim of this study is to characterize, purify and identify this gelatinase from T. gondii.First we characterized the 100 kDa-gelatinase secreted by T. gondii as an MMP-9-like (zinc metalloendopeptidase) but its activation process is different from human MMPs.Then, after the partial purification by a series of zinc-chelate chromatographies, we identified by mass spectrometry the gelatinase as the TGME49_227948 annotated in ToxoDB. This protease has M16C subfamily zinc-metalloprotease protein domains and is close to the 3D structure of the A chain of the 2FGE in Arabidopsis thaliana. In order to confirm the ToxoDB annotation, we sequenced the 5' end of the mRNA of this protease. Nevertheless our experimental results are not in the line with the predicted annotation in ToxoDB database.The amino acids sequence of this protease allowed us to synthesize two specific polyclonal antibodies in order to highlight two forms, 140 kDa and 100 kDa, and to emit the hypothesis that this protease could be cleaved to be activated. Moreover this metalloprotease was detected by Western Blot in the cytosol of the parasites but it can also be secreted in the conditioned medium. By immulocalization, the protease is present in the cytosol of the parasite without any preferential localization in a particular organelle.In this study, we showed that the parasitic gelatinase secreted by T. gondii could degrade extracellular matrix compounds, which could explain its potential role in the mechanism involved in the crossing of biological barriers
Alruhaili, M. H. B. "Genetic diversity of African isolates of Toxoplasma gondii." Thesis, University of Salford, 2016. http://usir.salford.ac.uk/37753/.
Повний текст джерелаFrohnecke, Nora. "Funktionelle Charakterisierung des Ferredoxin Redoxsystems von Toxoplasma gondii." Doctoral thesis, Humboldt-Universität zu Berlin, 2018. http://dx.doi.org/10.18452/19075.
Повний текст джерелаToxoplasmosis is one of the most common parasitic zoonoses world-wide, around 30% of human beings are infected. Toxoplasma gondii (phylum: Apicomplexa) contains a unique intracellular organelle derived from plastids, called apicoplast. The only known redox system in the apicoplast consists of the ferredoxin NADP+-reductase and its redox partner, ferredoxin (Fd). The latter donates electrons to different essential metabolic pathways in the apicoplast like the last two enzymes of the isoprenoid precursor biosynthesis and the lipoic acid synthesis. To dissect protein protein interactions for an electron transfer a bacterial reverse two hybrid system was used. The physical interaction of both proteins TgFd and TgLipA could be shown. Fd is supposed to play an important role in diverse metabolic pathways, hence a knock-out of the Fd gene is expected to generate a complex biochemical phenotype and be lethal to the parasite. Therefore two complementary approaches were used to analyze the role of TgFd in this context. The first strategy shall verify the essentiality of TgFd for the survival of T. gondii. It is based on the DiCre system whereby a defined genetic knock out of TgFd is produced. Respectives parasites have been generated, but at the end no genetic Fd knock out could be produced. In the second approach a conditional knock-down was generated, where the expression of the TgFd gene is repressed after induction. The Fd deficiency has wide ranging effects on T. gondii: The fatty acid synthesis of the apicoplast-synthesized fatty acids is reduced as well as the motility is decreased due to an affected isoprenoid synthesis. In total this leads to a dramatic inhibition of parasite growth. Both metabolic pathways depend upon the electron carrier Fd and thus are affected by Fd deficiency. The results underline the essential role of the ferredoxin redoxsystem of T. gondii.
Dardé, Marie-Laure. "Contribution à la caractérisation de Toxoplasma Gondii : étude isoenzymatique." Limoges, 1990. http://www.theses.fr/1990LIMO101A.
Повний текст джерелаGastens, Martin. "Virulenz-assoziierte Proteine von Toxoplasma gondii Identifikation und funktionelle Charakterisierung /." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=968522270.
Повний текст джерелаAdjogblé, Koku Zikpi. "Biochemische und funktionelle Charakterisierung eines neuen "Dense-granules"- Proteins von Toxoplasma gondii: GRA9." [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971753792.
Повний текст джерела