Host immune responses in a non replication model of Toxoplasma gondii infection.

2007 ◽  
Author(s):  
Jason P. Gigley
Keyword(s):  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Host Immune Responses ◽  
Replication Model ◽  
Toxoplasma Gondii Infection

scholarly journals Acute and Chronic Phases of Toxoplasma gondii Infection in Mice Modulate the Host Immune Responses

1998 ◽  
Vol 66 (6) ◽  
pp. 2991-2995 ◽  
Author(s):  
T. D. Nguyen ◽  
G. Bigaignon ◽  
J. Van Broeck ◽  
M. Vercammen ◽  
T. N. Nguyen ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Soluble Protein ◽  
Chronic Phase ◽  
Antibody Responses ◽  
Protein Antigen ◽  
Host Immune Responses ◽  
Toxoplasma Gondii Infection ◽  
Igg1 Isotype ◽  
Murine Antibody

ABSTRACT Murine antibody responses to soluble proteins are generally restricted to the immunoglobulin G1 (IgG1) isotype. When mice were infected with Toxoplasma gondii Beverley and concomitantly immunized with a soluble unrelated protein antigen, a modification in the isotypic distribution of antibodies directed against this nonparasite antigen was observed, with a preferential production of IgG2a. Interestingly, when mice were immunized with a soluble protein antigen during the chronic phase (day 40) of infection with T. gondii Beverley, a similar modification in the isotypic distribution of antiprotein antibodies was observed.

scholarly journals Innate, adaptive, and cell-autonomous immunity against Toxoplasma gondii infection

2019 ◽  
Vol 51 (12) ◽  
pp. 1-10 ◽  
Author(s):  
Miwa Sasai ◽  
Masahiro Yamamoto
Keyword(s):  
Immune Response ◽  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Parasitophorous Vacuole ◽  
Interferon Γ ◽  
Protective Role ◽  
Ifn Γ ◽  
Acquired Immune Responses ◽  
Toxoplasma Gondii Infection ◽  
Antimicrobial Immunity

AbstractHosts have been fighting pathogens throughout the evolution of all infectious diseases. Toxoplasma gondii is one of the most common infectious agents in humans but causes only opportunistic infection in healthy individuals. Similar to antimicrobial immunity against other organisms, the immune response against T. gondii activates innate immunity and in turn induces acquired immune responses. After activation of acquired immunity, host immune cells robustly produce the proinflammatory cytokine interferon-γ (IFN-γ), which activates a set of IFN-γ-inducible proteins, including GTPases. IFN-inducible GTPases are essential for cell-autonomous immunity and are specialized for effective clearance and growth inhibition of T. gondii by accumulating in parasitophorous vacuole membranes. Recent studies suggest that the cell-autonomous immune response plays a protective role in host defense against not only T. gondii but also various intracellular bacteria. Moreover, the negative regulatory mechanisms of such strong immune responses are also important for host survival after infection. In this review, we will discuss in detail recent advances in the understanding of host defenses against T. gondii and the roles played by cell-autonomous immune responses.

scholarly journals Transcriptome Analysis of Mouse Brain Infected with Toxoplasma gondii

2013 ◽  
Vol 81 (10) ◽  
pp. 3609-3619 ◽  
Author(s):  
Sachi Tanaka ◽  
Maki Nishimura ◽  
Fumiaki Ihara ◽  
Junya Yamagishi ◽  
Yutaka Suzuki ◽  
...  
Keyword(s):  
Gene Expression ◽  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Mouse Brain ◽  
Transcriptome Analysis ◽  
Host Cells ◽  
Content Type ◽  
Host Immune Responses ◽  
Wide Range ◽  
The Brain

ABSTRACTToxoplasma gondiiis an obligate intracellular parasite that invades a wide range of vertebrate host cells. Chronic infections withT. gondiibecome established in the tissues of the central nervous system, where the parasites may directly or indirectly modulate neuronal function. However, the mechanisms underlying parasite-induced neuronal disorder in the brain remain unclear. This study evaluated host gene expression in mouse brain following infection withT. gondii. BALB/c mice were infected with the PLK strain, and after 32 days of infection, histopathological lesions in the frontal lobe were found to be more severe than in other areas of the brain. Total RNA extracted from infected and uninfected mouse brain samples was subjected to transcriptome analysis using RNA sequencing (RNA-seq). In theT. gondii-infected mice, 935 mouse brain genes were upregulated, whereas 12 genes were downregulated. GOstat analysis predicted that the upregulated genes were primarily involved in host immune responses and cell activation. Positive correlations were found between the numbers of parasites in the infected mouse brains and the expression levels of genes involved in host immune responses. In contrast, genes that had a negative correlation with parasite numbers were predicted to be involved in neurological functions, such as small-GTPase-mediated signal transduction and vesicle-mediated transport. Furthermore, differential gene expression was observed between mice exhibiting the clinical signs of toxoplasmosis and those that did not. Our findings may provide insights into the mechanisms underlying neurological changes duringT. gondiiinfection.

Host immune responses to Toxoplasma gondii

2018 ◽  
Vol 30 (3) ◽  
pp. 113-119 ◽  
Author(s):  
Miwa Sasai ◽  
Ariel Pradipta ◽  
Masahiro Yamamoto
Keyword(s):  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Host Immune Responses

scholarly journals Chronic Toxoplasma gondii Infection Alleviates Experimental Autoimmune Encephalomyelitis by the Immune Regulation Inducing Reduction in IL-17A/Th17 Via Upregulation of SOCS3

2020 ◽  
Author(s):  
Do-Won Ham ◽  
Sang-Gyun Kim ◽  
Seung-Hwan Seo ◽  
Ji-Hun Shin ◽  
Sang Hyung Lee ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Responses ◽  
Th17 Cells ◽  
Cell Activation ◽  
Dependent Manner ◽  
Autoimmune Encephalomyelitis ◽  
Socs3 Expression ◽  
Toxoplasma Gondii Infection ◽  
Experimental Autoimmune

AbstractExperimental autoimmune encephalomyelitis (EAE) is a mouse model of multiple sclerosis (MS), a demyelinating autoimmune disease caused by the infiltration of a harmful autoreactive Th1 and Th17 cells. To mitigate MS, which is impossible to cure with medication only, immunomodulatory interventions that prevent Th17 cell activation are ideal. The objective of the present study was to analyze the effect of Toxoplasma gondii infection on the onset of EAE. Our results found that Toxoplasma gondii infection in the brain increases SOCS3 expression and decreases the phosphorylation of STAT3, resulting in reducing IL-17A and IL-23, which suppress the differentiation and expansion of pathogenic Th17 cells, an important factor in MS development. These immune responses resulted in a reduction in the clinical scoring of EAE induced by myelin oligodendrocyte glycoprotein 35–55 immunization. In the EAE group with T. gondii infection (Tg + EAE group), Th17-related immune responses that exacerbate the onset of EAE were reduced compared to those in the EAE group. This study suggests that the alleviation of EAE after T. gondii infection is regulated in a SOCS3/STAT3/IL-17A/blood–brain barrier integrity-dependent manner. Although parasite infection would not be permitted for MS treatment, this study using T. gondii infection identified potential targets that contribute to disease attenuation.

scholarly journals Selective and strain-specific NFAT4 activation by the Toxoplasma gondii polymorphic dense granule protein GRA6

2014 ◽  
Vol 211 (10) ◽  
pp. 2013-2032 ◽  
Author(s):  
Ji Su Ma ◽  
Miwa Sasai ◽  
Jun Ohshima ◽  
Youngae Lee ◽  
Hironori Bando ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Dense Granule ◽  
Type I ◽  
Dependent Manner ◽  
Activated T Cells ◽  
Host Immune Responses ◽  
Dense Granules ◽  
Granule Protein ◽  
C Terminus ◽  
Toxoplasma Gondii Infection

Toxoplasma gondii infection results in co-option and subversion of host cellular signaling pathways. This process involves discharge of T. gondii effector molecules from parasite secretory organelles such as rhoptries and dense granules. We report that the T. gondii polymorphic dense granule protein GRA6 regulates activation of the host transcription factor nuclear factor of activated T cells 4 (NFAT4). GRA6 overexpression robustly and selectively activated NFAT4 via calcium modulating ligand (CAMLG). Infection with wild-type (WT) but not GRA6-deficient parasites induced NFAT4 activation. Moreover, GRA6-deficient parasites failed to exhibit full virulence in local infection, and the treatment of WT mice with an NFAT inhibitor mitigated virulence of WT parasites. Notably, NFAT4-deficient mice displayed prolonged survival, decreased recruitment of CD11b+ Ly6G+ cells to the site of infection, and impaired expression of chemokines such as Cxcl2 and Ccl2. In addition, infection with type I parasites culminated in significantly higher NFAT4 activation than type II parasites due to a polymorphism in the C terminus of GRA6. Collectively, our data suggest that GRA6-dependent NFAT4 activation is required for T. gondii manipulation of host immune responses to maximize the parasite virulence in a strain-dependent manner.

scholarly journals Infection With Trypanosoma Lewisi or Trypanosoma Musculi May Promote The Spread of Toxoplasma Gondii

2020 ◽  
Author(s):  
Jiang-Mei Gao ◽  
Si-Qi Yi ◽  
Guo-Qing Geng ◽  
Zhi-Shen Xu ◽  
Geoff Hide ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Immune Status ◽  
Peritoneal Macrophages ◽  
No Production ◽  
Host Immune Responses ◽  
Trypanosoma Lewisi ◽  
Almost All ◽  
Globally Distributed ◽  
Laboratory Models

Abstract Background: Toxoplasma gondii can infect almost all warm-blooded vertebrates with pathogensis being largely influenced by the host immune status. As important epidemiological hosts, rodents are globally distributed and are also commonly found infected with haemoflagellates, such as those in the genus Trypanosoma. We here address whether and how co-infection with trypanosomes can influence T. gondii infection in laboratory models. Results: Rats of five strains, co-infected with T. lewisi, and mice of four strains, co-infected with T. musculi, were found to be more or less susceptible to T. gondii infection, respectively, with corresponding increased or decreased brain cyst burdens. Down-regulation of iNOS expression and decreased NO production or reverse were observed in the peritoneal macrophages of rats or mice, infected with trypanosomes, respectively.Conclusions: Trypanosoma lewisi and T. musculi can modulate host immune responses, either by enhancement or suppression, and influence the outcome of Toxoplasma infection.

scholarly journals Adjuvantic cytokine IL-33 improves the protective immunity of cocktailed DNA vaccine of ROP5 and ROP18 against toxoplasma gondii infection in mice

Parasite ◽  
2020 ◽  
Vol 27 ◽  
pp. 26 ◽  
Author(s):  
Yu-Chao Zhu ◽  
Yong He ◽  
Jian-Fa Liu ◽  
Jia Chen
Keyword(s):  
Toxoplasma Gondii ◽  
Immune Responses ◽  
Dna Vaccine ◽  
High Dose ◽  
Dna Immunization ◽  
Lethal Challenge ◽  
Molecular Adjuvant ◽  
Cell Immunity ◽  
Toxoplasma Gondii Infection ◽  
Immune Efficacy

Toxoplasma gondii is a threat for immunocompromized individuals, and no treatment is available for enhancing immunity against infection. Molecular adjuvants may improve the efficacy of DNA vaccine-induced T cell immunity. Here, we report that cocktailed DNA immunization with ROP5 and ROP18 boosted immune responses induced by a single DNA immunization with ROP5 or ROP18, but also that co-administration of molecular adjuvant IL-33 enhanced immune efficacy induced by this cocktailed DNA vaccination. These improved immune responses were characterized by higher Toxoplasma-specific IgG2a titers, Th1 responses associated with the production of IFN-γ, IL-2, IL-12, as well as cell-mediated activity with higher frequencies of CD8+ and CD4+ T cells. More importantly, this enhanced immunity has the ability to confer remarkable protection against a high dose lethal challenge of the T. gondii RH strain and thus against chronic infection with the T. gondii PRU strain. These data show that IL-33 is a promising immunoadjuvant to facilitate humoral as well as cellular immunity in a vaccine setting against T. gondii, and suggest that it should be evaluated in strategies against other apicomplexan parasites.

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