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314 results for “Toxoplasma gondii”
Proteomic characterization of Toxoplasma gondii ME49 derived strains resistant to the artemisinin derivatives artemiside and artemisone
<p>Full datasets of proteomes of artemisone (GC003) and artemiside (GC008) resistant T. gondii Me49 strains.</p> <p>Paper submitted to International Journal of Parasitology-Drugs and Drug Resistance</p> <p>Differential proteomic analysis of the artemisone (GC003<sup>R</sup>) and artemiside (GC008<sup>R</sup>) resistant strains versus their corresponding <em>T. gondii</em> ME49 wildtype yielded 3977 unique peptides matching to 733 <em>T. gondii</em> proteins. The complete dataset is available as supplemental Table S1. A more detailed analysis revealed that 215 proteins were significantly downregulated in GC003R and 8 proteins in GC008R as compared to their wildtype ME49. Two proteins were downregulated in both strains. No proteins were upregulated in the resistant strains as compared to their corresponding wildtype. The complete list of the differentials is given as supplemental Table S2. </p>
Fig. 1 in Foxes (Vulpes vulpes) as sentinels for parasitic zoonoses, Toxoplasma gondii and Trichinella nativa, in the northeastern Canadian Arctic
Fig. 1. Map of Nunavik (© Lemire et al., 2015).
Towards a rapid sequencing-based molecular surveillance and mosaicism investigation of Toxoplasma gondii (nucleotide alignment dataset)
<p>This dataset includes the nucleotide alignment of eight Toxoplasma gondii genome loci (Sag1 / Chromossome VIII, Gra6 / Chromossome X, PK1 / Chromossome VI, Sag3 / Chromossome XII, L363 / Chromossome VIIb, CB21-4 / Chromossome III, M102 / Chromossome VIIa, Sag2 / Chromossome VIII). Each alignment includes sequences from T. gondii reference strains (retrieved from ToxoDB) as well as sequences from multiple clinical strains (obtained by Sanger / Next-generation sequencing) of the collection of the National Reference Laboratory of Parasitic and Fungal Infections, Department of Infectious Diseases, National Institute of Health Dr. Ricardo Jorge, Portugal. </p>
Fig. 1 in Toxoplasma gondii in Australian macropods (Macropodidae) and its implication to meat consumption
Fig. 1. Flowchart of article selection.
Fig. 1 in Sentinels in the shadows: Exploring Toxoplasma gondii and other Sarcocystidae parasites in synanthropic rodents and their public health implications
Fig. 1. Geographical distribution of PCR positive rodents.
More people, more cats, more parasites: Human population density and temperature variation predict the prevalence of Toxoplasma gondii oocyst shedding in free-ranging domestic and wild felids
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A single-parasite transcriptional atlas of Toxoplasma gondii reveals novel control of antigen expression
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Data from: Defining the risk landscape in the context of pathogen pollution: Toxoplasma gondii in sea otters along the Pacific Rim
Pathogens entering the marine environment as pollutants exhibit a spatial signature driven by their transport mechanisms. The sea otter (Enhydra lutris), a marine animal that lives much of its life within sight of land, presents a unique opportunity to understand land-sea pathogen transmission. Using a dataset on Toxoplasma gondii prevalence across sea otter range from Alaska to California, we found that the dominant drivers of infection risk vary depending upon the spatial scale of analysis. At the population level, regions with high T. gondii prevalence had higher human population density and a greater proportion of human-dominated land uses suggesting a strong role for population density of the felid definitive host of this parasite. This relationship persisted when a subset of data were analysed at the individual level: large-scale patterns in sea otter T. gondii infection prevalence were largely explained by individual exposure to areas of high human housing unit density, and other landscape features associated with anthropogenic land use, such as impervious surfaces and cropping land. These results contrast with the small-scale, within-region analysis, in which age, sex and prey choice accounted for most of the variation in infection risk, and terrestrial environmental features provided little variation to help in explaining observed patterns. These results underscore the importance of spatial scale in study design when quantifying both individual-level risk factors and landscape-scale variation in infection risk.
Interaction of diet and habitat predicts Toxoplasma gondii infection rates in wild birds at a global scale
<p><b>Aim:</b> Free-ranging wildlife are valuable sentinels for zoonotic, multi-host pathogens, and novel insight on parasite transmission patterns is possible through a macroecological approach. <i>Toxoplasma gondii</i> is a protozoan capable of infecting all warm-blooded animals, including humans, primarily through a free-living oocyst and/or tissue cyst life-stage. Anthropogenic disturbance is facilitating the spread of <i>T. gondii</i>, making it critical to understand the general ecological and life history drivers of <i>T. gondii</i> infections in wild birds, which are important intermediate hosts. Our goal was to determine how habitat (terrestrial vs. aquatic), dietary trophic level and scavenging behaviour influence <i>T. gondii</i> infection prevalence in wild birds on a global scale.</p> <p><b>Location: </b>Global</p> <p><b>Time period: </b>1952-2017</p> <p><b>Major taxa studied: </b>Birds</p> <p><b>Methods</b>: Our analysis used the serological, bioassay and molecular prevalence data of <i>T. gondii</i> in avian species compiled from 81 studies conducted worldwide and encompassing 24,344 individuals from 393 avian species from 84 families.</p> <p><b>Results: </b>We show that at a global scale, trophic level and habitat significantly interact to influence <i>T. gondii </i>prevalence in avian intermediate hosts. In the terrestrial environment, <i>T. gondii</i> prevalence increases with trophic level, consistent with predominant tissue cyst transmission. The highest prevalence was in terrestrial omnivores, which may reflect their synanthropic foraging behaviour. In aquatic species, prevalence was more consistent across trophic levels, but high prevalence in aquatic herbivores and insectivores reflects significant waterborne exposure to oocysts. Contrary to our predictions, generalized scavenging <i>per se</i> was not associated with increased prevalence.</p> <p><b>Main conclusions:</b> This study highlights the value of comparing pathogen prevalence among multiple ecological guilds and ecosystem types for a comprehensive understanding of the epidemiology of generalist pathogens, such as <i>T. gondii</i>. Increased effort is needed to reduce <i>T. gondii</i> spillover from the domestic cat cycle into wildlife populations.</p>
Contrasting disease progression, microglia reactivity, tolerance, and resistance to Toxoplasma gondii infection in two mouse strains
<p><strong><span>Figure S1</span></strong><span>. Stereological Sampling: Low-power photomicrographs (A and B) displaying the molecular layer of the dentate gyrus, the area of interest, alongside the sampling grid (C). Additionally, a high-power photomicrograph (D) showcases IBA-1 immunolabeled microglia (the object of interest). Scale bar: A - 250µm, and D: 25µm.</span></p> <p> </p> <p><strong><span>Figure S2</span></strong><span>. The recovery of BALB/c microglia in the molecular layer of dentate gyrus was observed 43 days after infection. At this point, only minor morphological changes were observed, and all the morphological changes induced by <em>T. gondii</em> infection at 22 dpi have disappeared. The analysis methods used included hierarchical cluster analysis (A), discriminant function analysis (C and E), morphological complexity (B), and convex hull volume (D).</span></p>
An extended epiphenotype for an extended phenotype in Toxoplasma gondii infected feral house mice
<p>Parasitism of mice by Toxoplasma gondii reduces the host's aversion to cat odors, likely increasing predation and transmission of the parasite to its definitive host. This behavioral change suggests a parasitic manipulation where host behavior becomes an extended phenotype of the parasite. Independently, epigenetic changes within an organism are now known to create behavioral change. The results described here provide an experimental connection between these disparate strands of extended phenotypes and the role of epigenetics in behavioral diversity. Using mice captured on Kangaroo Island in Australia, we demonstrate that Toxoplasma gondii infection leads to specific DNA hypomethylation events in the host brain. Previous laboratory studies have shown that these epigenetic changes underlie the central processing of cat odors. We posit that the concept of extended phenotype can be expanded to extended epiphenotype, thus linking parasite genes to host behavior through epigenesis. This phenomenon has broad implications for inter-species relationships.</p>
Tim-3 regulates the immunosuppressive function of decidual MDSCs via the Fyn-STAT3-C/EBPβ pathway during Toxoplasma gondii infection
<p><span>Myeloid-derived suppressor cells (MDSCs) play a key role in maintaining maternal-fetal tolerance for a successful pregnancy, but the role of MDSCs in abnormal pregnancy caused by <em>Toxoplasma</em> <em>gondii</em> infection is unknown. Herein, we revealed a distinct mechanism by which T-cell immunoglobulin domain- and mucin domain-containing protein-3 (Tim-3), an immune checkpoint receptor that balances maternal-fetal tolerance during pregnancy, contributes to the immunosuppressive function of MDSCs during <em>T. gondii</em> infection. The expression of Tim-3 in decidual MDSCs was significantly </span><span>downregulated</span><span> following <em>T. gondii </em>infection. The proportion of monocytic </span><span>MDSC</span><span> population, the inhibitory effect of MDSCs on T-cell proliferation, the levels of STAT3 phosphorylation, and the expression of functional molecules (Arg-1 and IL-10) in MDSCs were all decreased in <em>T. gondii</em>-infected pregnant Tim-3 gene knockout (Tim-3KO) mice compared with infected pregnant WT mice. After treatment with Tim-3-neutralizing Ab <em>in vitro</em>, the expression levels of Arg-1, IL-10, C/EBPβ, and p-STAT3 were decreased, the interaction between Fyn and Tim-3 or between Fyn and STAT3 </span><span>was</span><span> weakened,</span><span> and</span><span> the binding ability of C/EBPβ to the promoters of <em>ARG1</em> and <em>IL10</em> </span><span>was</span><span> decreased in human decidual MDSCs with <em>T. gondii</em> infection, while opposite results were observed following treatment with galectin-9 (a ligand for Tim-3). </span><span>Inhibitors</span><span> of Fyn and STAT3 also </span><span>downregulated</span><span> the expression of Arg-1 and IL-10 in decidual MDSCs and exacerbated adverse pregnancy outcomes caused by <em>T. gondii</em> infection in mice. Therefore, our studies discovered that the decrease of Tim-3 after <em>T. gondii</em> infection could downregulate the functional molecules of Arg-1 and IL-10 expression in decidual MDSCs through the Fyn-STAT3-C/EBPβ signaling pathway and weaken their immunosuppressive function, which eventually contributes to the development of adverse pregnancy outcomes.</span></p>
A German Multicenter Study on Toxoplasma Gondii in First-episode Schizophrenia
ClinicalTrials.gov study NCT00686400. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Toxoplasma Gondii Infection in Both Children and Adult Patients With Hematological Malignancies
ClinicalTrials.gov study NCT05963295. IPD Sharing: UNDECIDED. Countries: 1. Publications: 4.
A Randomized Prospective Study of Pyrimethamine Therapy for Prevention of Toxoplasmic Encephalitis in HIV-Infected Individuals With Serologic Evidence of Latent Toxoplasma Gondii Infection
ClinicalTrials.gov study NCT00000666. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Interaction of diet and habitat predicts Toxoplasma gondii infection rates in wild birds at a global scale
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Data from: Defining the risk landscape in the context of pathogen pollution: Toxoplasma gondii in sea otters along the Pacific Rim
Open the record for dataset details and reuse information.
An extended epiphenotype for an extended phenotype in Toxoplasma gondii infected feral house mice
Open the record for dataset details and reuse information.
Tim-3 regulates the immunosuppressive function of decidual MDSCs via the Fyn-STAT3-C/EBPβ pathway during Toxoplasma gondii infection
Open the record for dataset details and reuse information.
Data from: Proteome-wide lysine acetylation in cortical astrocytes and alterations that occur during infection with brain parasite Toxoplasma gondii
Lysine acetylation is a reversible post-translational modification (PTM) that has been detected on thousands of proteins in nearly all cellular compartments. The role of this widespread PTM has yet to be fully elucidated, but can impact protein localization, interactions, activity, and stability. Here we present the first proteome-wide survey of lysine acetylation in cortical astrocytes, a subtype of glia that is a component of the blood-brain barrier and a key regulator of neuronal function and plasticity. We identified 529 lysine acetylation sites across 304 proteins found in multiple cellular compartments that largely function in RNA processing/transcription, metabolism, chromatin biology, and translation. Two hundred and seventy-seven of the acetylated lysines we identified on 186 proteins have not been reported previously in any other cell type. We also mapped an acetylome of astrocytes infected with the brain parasite, Toxoplasma gondii. It has been shown that infection with T. gondii modulates host cell gene expression, including several lysine acetyltransferase (KAT) and deacetylase (KDAC) genes, suggesting that the host acetylome may also be altered during infection. In the T. gondii-infected astrocytes, we identified 34 proteins exhibiting a level of acetylation >2-fold and 24 with a level of acetylation <2-fold relative to uninfected astrocytes. Our study documents the first acetylome map for cortical astrocytes, uncovers novel lysine acetylation sites, and demonstrates that T. gondii infection produces an altered acetylome.
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