AMA1-Deficient Toxoplasma gondii Parasites Transiently Colonize Mice and Trigger an Innate Immune Response That Leads to Long-Lasting Protective Immunity

Lagal, Vanessa; Dinis, Márcia; Cannella, Dominique; Bargieri, Daniel Youssef; Gonzalez, Virginie; Andenmatten, Nicole; Meissner, Markus; Tardieux, Isabelle

doi:10.1128/iai.02606-14

Cited by 21 publications

(15 citation statements)

References 54 publications

(56 reference statements)

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“…Toward this aim, we used an image flow cytometry (IFC) platform to collect data on large populations of Mimivirus ‐infected cells. Recent works have used IFC to study infection by the intracellular pathogens Leishmania amazonensis , Toxoplasma gondii , Blastocystis , Mycobacterium tuberculosis , and Plasmodium falciparum . The current study is the first, to the best of our knowledge, to monitor a viral pathogen by IFC and to follow the kinetics of various intracellular processes associated with viral takeover of the cell.…”

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confidence: 98%

Kinetics of Mimivirus Infection Stages Quantified Using Image Flow Cytometry

et al. 2019

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Due to the heterogeneity of viruses and their hosts, a comprehensive view of viral infection is best achieved by analyzing large populations of infected cells. However, information regarding variation in infected cell populations is lost in bulk measurements. Motivated by an interest in the temporal progression of events in virally infected cells, we used image flow cytometry (IFC) to monitor changes in Acanthamoeba polyphaga cells infected with Mimivirus . This first use of IFC to study viral infection required the development of methods to preserve morphological features of adherent amoeba cells prior to detachment and analysis in suspension. It also required the identification of IFC parameters that best report on key events in the Mimivirus infection cycle. The optimized IFC protocol enabled the simultaneous monitoring of diverse processes including generation of viral factories, transport, and fusion of replication centers within the cell, accumulation of viral progeny, and changes in cell morphology for tens of thousands of cells. After obtaining the time windows for these processes, we used IFC to evaluate the effects of perturbations such as oxidative stress and cytoskeletal disruptors on viral infection. Accurate dose‐response curves could be generated, and we found that mild oxidative stress delayed multiple stages of virus production, but eventually infection processes occurred with approximately the same amplitudes. We also found that functional actin cytoskeleton is required for fusion of viral replication centers and later for the production of viral progeny. Through this report, we demonstrate that IFC offers a quantitative, high‐throughput, and highly robust approach to study viral infection cycles and virus–host interactions. © The Authors. Cytometry Part A published by Wiley Periodicals, Inc. on behalf of International Society for Advancement of Cytometry.

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confidence: 98%

Kinetics of Mimivirus Infection Stages Quantified Using Image Flow Cytometry

et al. 2019

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“…Recently, a pioneering study has investigated the metabolic needs and capabilities of T. gondii using a combined computational and experimental approach 10 . The interplay between T. gondii parasites and their hosts has been studied for decades using targeted approaches, such as the analysis of mutants or host immunological responses 11 12 . Although much has been learned from such studies, they focus on individual pathways and fail to reveal the global effects of infection on the host’s metabolism.…”

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Metabolomic Profiling of Mice Serum during Toxoplasmosis Progression Using Liquid Chromatography-Mass Spectrometry

Zhou

Elsheikha

et al. 2016

Sci Rep

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Better understanding of the molecular changes associated with disease is essential for identifying new routes to improved therapeutics and diagnostic tests. The aim of this study was to investigate the dynamic changes in the metabolic profile of mouse sera during T. gondii infection. We carried out untargeted metabolomic analysis of sera collected from female BALB/c mice experimentally infected with the T. gondii Pru strain (Genotype II). Serum samples were collected at 7, 14 and 21 day post infection (DPI) from infected and control mice and were subjected to liquid chromatography-quadrupole time-of-flight mass spectrometry (LC-Q-TOF-MS)-based global metabolomics analysis. Multivariate statistical analysis identified 79 differentially expressed metabolites in ESI+ mode and 74 in ESI− mode in sera of T. gondii-infected mice compared to the control mice. Further principal component analysis (PCA) and partial least squares-discrimination analysis (PLS-DA) identified 19 dysregulated metabolites (5 in ESI+ mode and 14 in ESI− mode) related to the metabolism of amino acids and energy metabolism. The potential utility of these metabolites as diagnostic biomarkers was validated through receiver operating characteristic (ROC) curve analysis. These findings provide putative metabolite biomarkers for future study and allow for hypothesis generation about the pathophysiology of toxoplasmosis.

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“…For instance, previous reports have shown that antibodies against AMA1 or small specific AMA1-binding peptides inhibit the invasion of host cells by Toxoplasma, E. tenella, Babesia, Neospora, and Plasmodium [3,[8][9][10][11]. AMA1 is also a long-standing effective candidate vaccine for some apicomplexans, including N. caninum, T. gondii and Plasmodium [11][12][13]. In Toxoplasma and Plasmodium, AMA1 is reportedly involved in apical reorientation [14], host-cell attachment [7,15], invasion and establishment of the moving-junction [16], , and the provision of a signal that initiates intracellular replication [17].…”

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Eimeria tenella Eimeria-specific protein that interacts with apical membrane antigen 1 (EtAMA1) is involved in host cell invasion

Cong

Zhao

Zhu

et al. 2020

Preprint

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Background: Avian coccidiosis is a widespread, economically significant disease of poultry, caused by several species of the protozoan parasite Eimeria. Among these species, E. tenella causes hemorrhagic pathologies and high mortality. These parasites have complex and diverse lifestyles that require the invasion of their host cells. This is mediated by various proteins secreted from apical secretory organelles. Apical membrane antigen 1 (AMA1), which is released from micronemes and is conserved across all apicomplexans, plays a central role in the host cell invasion. In a previous study, some putative EtAMA1-interacting proteins of E. tenella were screened. In this study, we characterized one putative EtAMA1-interacting protein, E. tenella Eimeria -specific protein (EtEsp).Methods: Bimolecular fluorescence complementation (BiFC) and glutathione S-transferase (GST) fusion protein pull-down (GST pull-down) were used to confirm the interaction between EtAMA1 and EtEsp in vivo and in vitro. The expression of EtEsp was analyzed in different developmental stages of E. tenella with quantitative PCR and western blotting. The secretion of EtEsp protein was tested with staurosporine when sporozoites were incubated in complete medium at 41 °C.The localization of EtEsp was analyzed with an immunoﬂuorescence assay. An in vitro invasion inhibition assay was conducted to assess the ability of antibodies against EtEsp to inhibit cell invasion by E. tenella sporozoites.Results: The interaction between EtAMA1 and EtEsp was confirmed with BiFC in vivo and by GST pull-down in vitro. Our results show that EtEsp is differentially expressed during distinct phases of the parasite life cycle. An immunoﬂuorescence analysis showed that the EtEsp protein is mainly distributed on the parasite surface, and that the expression of this protein increases during the development of the parasite in the host cells. Using staurosporine, we showed that EtEsp is a secreted protein, but not from micronemes. In inhibition tests, a polyclonal anti-rEtEsp antibody attenuated the capacity of E. tenella to invade host cells in vitro. Conclusion: In this study, we show that EtEsp interacts with EtAMA1 and that the protein is secreted protein, but not from micronemes. The protein participates in the sporozoite invasion of host cells and maybe involved in the growth of the parasite in the host. These data have implications for the use of EtAMA1 or EtAMA1-interacting proteins as targets in intervention strategies against avian coccidiosis.

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AMA1-Deficient Toxoplasma gondii Parasites Transiently Colonize Mice and Trigger an Innate Immune Response That Leads to Long-Lasting Protective Immunity

Cited by 21 publications

References 54 publications

Kinetics of Mimivirus Infection Stages Quantified Using Image Flow Cytometry

Kinetics of Mimivirus Infection Stages Quantified Using Image Flow Cytometry

Metabolomic Profiling of Mice Serum during Toxoplasmosis Progression Using Liquid Chromatography-Mass Spectrometry

Eimeria tenella Eimeria-specific protein that interacts with apical membrane antigen 1 (EtAMA1) is involved in host cell invasion

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