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

ABSTRACT: 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. Bone marrow-derived macrophages (BMMs) from mLys-Mcre Stat3fl/fl mice were infected with type II (Pru A7), type II +ROP16 I, type II Δgra15, or type II Δgra15 + ROP16I and gene expression was analyzed 18 hrs after infection. This data set was generated side by side with infections performed in B6 BMDMs, the gene expression results for that experiment were previoiusly submitted under the GEO accession number GSE29404. In addition, gene expression of wild type B6 and Stat6-/- BMDMs were infected with the II+ROP16I strain.

ORGANISM(S): Mus musculus

SUBMITTER: Kirk Jensen

PROVIDER: E-GEOD-45309 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

Gene expression profiles of the small intestine and Peyer's patches from mice that were orally infected with Toxoplasma

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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 Δgra15, or type II Δgra15 + ROP16I.

2011-05-20 | GSE29404 | GEO

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

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

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

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.

2019-11-22 | GSE140772 | GEO

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

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Gene expression profiles of the small intestine and Peyer's patches from mice that were orally infected with Toxoplasma

Project description:The Toxoplasma type I ROP16 kinase directly activates the host STAT3 and STAT6 transcription factors and when transgenically expressed in the orally virulent type II strain, promotes host resistance to oral challenge. The transcriptional profile of type II and II+ROP16I infected Peyer's patches and intestines from orally infected mice on day 5 was determined to elucidate host signaling pathways and molecular gene targets that correlate with protective immunity in the gut of orally challenged animals C57BL/6 female mice were orally gavaged with 1000 tissue cysts of the type II or II+ROP16I strain. On Day 5 of infection the Peyer's patches and intestines were analyzed for parasite burden by bioluminescence imaging. Individual Peyer's patches and intestinal sections, corresponding to the middle third of the intestine (~jejunum), that had equivalent parasite burden were snap frozen in liquid nitrogen. The samples were crushed using a sterile 16 G needle in tubes on dry ice. In the case of the intestine, the sample was resuspended in TRizol, extruded through a needle using a syringe and RNA was isolated according to manufacturer's protocol; for the Peyer's patch, the sample was suspended in cell lysis buffer and RNA isolated using the RNeasey kit (Invitrogen) according to the manufacter's protocol.

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RNAseq Reveals Virulence-Specific Host Responses to M. tuberculosis infection

Project description:We infect bone marrow derived macrophages (BMDMs) with either a Hyper or Hypovirulent Mycobacterium tuberculolsis strain and assess the host response to these bacteria through RNAseq Uninfected BMDMs served as controls, BMDMs infected with Hypervirulent M.tb (designated R55), BMDMs infected with Hypovirulent m.tb (designated R50). 3 groups with 3 biological replicates, each analysed in triplicate.

2016-03-01 | E-GEOD-78706 | biostudies-arrayexpress

Arginine utilization following mycobacteria infection in macrophages is dependent on autocrine-paracrine signaling

Project description:Nitric oxide (NO) produced by macrophages (MØs) is toxic to both host tissues and invading pathogens and its regulation is therefore essential to suppress host cytotoxicity. MØ arginase 1 (Arg1) inhibits NO production by competing with NO synthases for arginine, the common substrate of NO synthases and arginases. Two signal transduction pathways control Arg1 expression in MØs. First, a MyD88-dependent pathway induces Arg1 in intracellular infections, while a second Stat6-dependent pathway is required for Arg1 expression in alternativelyactivated MØs. We found that mycobacteria-infected MØs produce soluble factors that induce Arg1 in an autocrine-paracrine manner via Stat3. We identify these factors as IL-6, IL-10 and GCSF. We further establish that Arg1 expression is controlled by the MyD88-dependent production of IL-6, IL-10 and G-CSF rather than cell intrinsic MyD88 signaling to Arg1. Our data reveal the MyD88-dependent pathway of Arg1induction following BCG infection requires Stat3 activation and may result in the development of an immunosuppressive niche in granulomas due to the induced Arg1 production in surrounding uninfected MØs We used microarrays to perform genome wide expression analysis in mycobacteria-infected macrophages from C57Bl/6 WT and MyD88-knockout mice.

2010-07-14 | E-GEOD-22935 | biostudies-arrayexpress

The Host Response to a Clinical MDR Mycobacterial Strain Cultured in a Detergent-Free Environment: A Global Transcriptomics Approach

Project description:We infect bone marrow derived macrophages (BMDMs) with Mycobacterium cultured with and without Tween 80 and asses the host response to these bacteria through RNAseq Uninfected BMDMs served as controls, BMDMs infected with detergent-free M.tb (designated RNT), BMDMs infected with Tween cultured m.tb (designated RT). 3 groups with 3 biological replicates, each analysed in triplicate.

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