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Unknown,Transcriptomics,Genomics,Proteomics

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ROP16-dependent host transcriptional responses in chicken embryonic fibroblasts infected with T. gondii [RH, ROP16-KO]

ABSTRACT: Toxoplasma gondii is a ubiquitous protozoan pathogen able to infect both mammalian and avian hosts. Surprisingly, just three strains appear to account for the majority of isolates from Europe and N. America. To test the hypothesis that strain divergence might be driven by differences between mammalian and avian response to infection, we examine in vitro strain-dependent host responses in a representative avian host, the chicken. To identify parasite drivers of strain-dependent host response, QTL mapping was used; analysis revealed a locus on Toxoplasma chromosome VIIb. To determine whether this was the parasite gene ROP16, array analysis was performed on chicken embryonic fibroblasts infected with Type I parasites and ROP16-KO parasites (of a Type I background). Chicken embryonic fibroblasts were cultivated in vitro and infected with either Type I (RH) parasites or Type I ROP16-KO parasites; ROP16-dependent host transcriptional responses were then analyzed at 5 hours post-infection.

ORGANISM(S): Gallus gallus

SUBMITTER: Yi-Ching Ong

PROVIDER: E-GEOD-29564 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ROP16-dependent host transcriptional responses in chicken embryonic fibroblasts infected with T. gondii [RH, ROP16-KO]

Project description:Toxoplasma gondii is a ubiquitous protozoan pathogen able to infect both mammalian and avian hosts. Surprisingly, just three strains appear to account for the majority of isolates from Europe and N. America. To test the hypothesis that strain divergence might be driven by differences between mammalian and avian response to infection, we examine in vitro strain-dependent host responses in a representative avian host, the chicken. To identify parasite drivers of strain-dependent host response, QTL mapping was used; analysis revealed a locus on Toxoplasma chromosome VIIb. To determine whether this was the parasite gene ROP16, array analysis was performed on chicken embryonic fibroblasts infected with Type I parasites and ROP16-KO parasites (of a Type I background).

2011-05-27 | GSE29564 | GEO

Host responses in chicken embryonic fibroblasts infected with different strains of Toxoplasma gondii [F1 progeny]

Project description:Toxoplasma gondii is a ubiquitous protozoan pathogen able to infect both mammalian and avian hosts. Surprisingly, just three strains appear to account for the majority of isolates from Europe and N. America. To test the hypothesis that strain divergence might be driven by differences between mammalian and avian response to infection, we examine in vitro strain-dependent host responses in a representative avian host, the chicken. Chicken embryonic fibroblasts were cultivated in vitro and infected with different strains of Toxoplasma gondii; host transcriptional responses were then analyzed at 24 hours post-infection.

2011-05-27 | E-GEOD-29563 | biostudies-arrayexpress

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2011-05-27 | E-GEOD-29562 | biostudies-arrayexpress

The Toxoplasma gondii virulence factor ROP16 acts in cis and trans and suppresses T cell responses [CEP_invivo_Ai6_1dpi]

Project description:The ability of Toxoplasma gondii to inject the rhoptry kinase ROP16 into host cells results in the activation of the transcription factors STAT3 and STAT6, but it is unclear how these events impact infection. Here, parasites that inject Cre-recombinase with rhoptry proteins were used to distinguish infected macrophages from those only injected with parasite proteins. Transcriptional profiling revealed that injection of rhoptry proteins alone was sufficient to induce an M2 phenotype that is dependent on STAT3 and STAT6, but only infected cells displayed reduced expression of anti-microbial genes and antigen presentation pathways. In vivo, the absence of STAT3 or STAT6 improved parasite control while the loss of ROP16 resulted in a marked reduction in parasite numbers and heightened parasite-specific T cell responses. Thus, ROP16 is a virulence factor that can act in cis and trans to promote M2 programs and which limits the magnitude of parasite-specific T cell responses.

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The Toxoplasma gondii virulence factor ROP16 acts in cis and trans and suppresses T cell responses [BMMC_invitro_stim_24hr]

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Expression data from RAW264.7 murine macrophages infected with Toxoplasma gondii and subsequently stimulated with interferon-gamma

Project description:Toxoplasma strains are known to inhibit the expression of several interferon-gamma induced genes, and a type II strain was shown to dysregulate genome-wide responses to interferon-gamma in human fibroblasts (Kim et al., 2007, J Immunol.). In this study we aimed to determine the effect of infection with three clonal lineages of Toxoplasma, type I, II, and III strains on genome-wide interferon-gamma induced transcription in murine macrophages. We also assessed the effect of the two main Toxoplasma modulators of mouse macrophage transcription, ROP16 and GRA15 (Jensen et al., 2011, Cell Host Microbe). We used Affymetrix microarrays to analyze host cell transcription after Toxoplasma infection and interferon-gamma stimulation. RAW264.7 murine macrophages were left uninfected or infected with type I (RH), type I ?rop16 (RH ?rop16), type II (Pru), type II ?gra15 (Pru ?gra15), or type II (CEP) parasites at an MOI ~5 for 18 hours and subsequently stimulated with murine IFN-? for six hours. Plaque assays were done to assess parasite viability. Total RNA was isolated and hybridized to Affymetrix Mouse 430A 2.0 gene chips.

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Host responses in chicken embryonic fibroblasts infected with different strains of Toxoplasma gondii [F1 progeny]

2011-05-27 | GSE29563 | GEO

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Expression Data from Toxoplasma gondii-Infected Murine Bone Marrow-Derived Macrophages

Project description:We wanted to determine how type II Toxoplasma GRA15 and type I ROP16 affect host gene expression. We infected bone marrow-derived macrophages (BMMs) from B6 mice with type II (Pru), type II +ROP16 I, type II ?gra15, or type II ?gra15 + ROP16I. BMMs were plated, then infected with parasites for 18 hours. RNA was harvested from the cells by Trizol.

2011-05-20 | E-GEOD-29404 | biostudies-arrayexpress

Gene expression Data from Toxoplasma gondii-Infected Murine Bone Marrow-Derived STAT6 and STAT3 Deficient Macrophages

Project description:The Toxoplasma type I ROP16 kinase directly activates the host STAT3 and STAT6 transcription factors and regulates the expression of many host genes. However, many of genes lack known STAT3/6 transcription factor binding sites in their promoter regions. We wanted to understand what fraction of host genes that are modulated by ROP16 were dependent on the STAT3 and STAT6 signaling pathways.

2013-03-20 | GSE45309 | GEO

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