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Gasdermin-D-dependent IL-1 alpha release from microglia promotes protective immunity during chronic Toxoplasma gondii infection

ABSTRACT: RNA-seq experiment on FACS-sorted microglial and macrophage cell populations (infected with T. gondii type II strain Me49)

ORGANISM(S): Mus musculus

PROVIDER: GSE146680 | GEO | 2020/03/10

REPOSITORIES: GEO

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Gasdermin-D-dependent IL-1α release from microglia promotes protective immunity during chronic Toxoplasma gondii infection.

Project description:Microglia, resident immune cells of the CNS, are thought to defend against infections. Toxoplasma gondii is an opportunistic infection that can cause severe neurological disease. Here we report that during T. gondii infection a strong NF-κB and inflammatory cytokine transcriptional signature is overrepresented in blood-derived macrophages versus microglia. Interestingly, IL-1α is enriched in microglia and IL-1β in macrophages. We find that mice lacking IL-1R1 or IL-1α, but not IL-1β, have impaired parasite control and immune cell infiltration within the brain. Further, we show that microglia, not peripheral myeloid cells, release IL-1α ex vivo. Finally, we show that ex vivo IL-1α release is gasdermin-D dependent, and that gasdermin-D and caspase-1/11 deficient mice show deficits in brain inflammation and parasite control. These results demonstrate that microglia and macrophages are differently equipped to propagate inflammation, and that in chronic T. gondii infection, microglia can release the alarmin IL-1α, promoting neuroinflammation and parasite control.

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Toxoplasma gondii ME49

Project description:Toxoplasma gondii ME49

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MicroRNA expression profile of porcine alveolar macrophages infected with Toxoplasma gondii

Project description:Purpose: Porcine alveolar macrophage was infected by T. gondii including Rh strain and Me49 strain. We want to explore the change of miRNAs after infected with T. gondii in porcine alveolar macrophages. Results: Our study generated six mi RNA expression profiles from macrophages which infect with Rh strain and Me49 and control group in different time. Compare with T. gondii-infected and uninfected with T. gondii, 81 differentially expressed mi RNAs were identified, including 36 novel mi RNAs and 45 mature mi RNAs.

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Toxoplasma gondii ME49

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Project description:Expression profile microarray of human foreskin fibroblast cell comparing control untreated HFF cell with HFF cell infected with ME49 strain.Study on Toxoplasma gondii infection of HFF cell LncRNAs expression, for further studies on the differential exprssion of LncRNAs in HFF cell against the infection of Toxoplasma gondii research provide the basic function.

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A novel nuclear protein complex controlling the expression of developmentally regulated genes in Toxoplasma gondii [RNA-seq]

Project description:To investigate the transcriptional effects of TgAP2XII-5 on type II Toxoplasma gondii (ME49) in the tachyzoite and bradyzoite stages. Also, to study the transcriptional role of TgAIP1 on ME49 tachyzoites.

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RESTRICTION checkpoint controls bradyzoite development in Toxoplasma gondii

Project description:The Toxoplasma gondii G1 RESTRICTION checkpoint operates the switch between parasite growth and differentiation. The Cdk-related G1 kinase TgCrk2 forms alternative complexes with atypical cyclins (TgCycP1, TgCycP2 and TgCyc5) in the rapidly dividing developmentally incompetent RH and slower dividing developmentally competent ME49 tachyzoites and bradyzoites. The TgCycP1 expression interferes with bradyzoite differentiation. The TgCycP2 regulates G1 in the developmentally competent ME49 but not in the developmentally incompetent RH tachyzoites. Examination of TgCycP2 and TgCyc5 in alkaline induced and spontaneous bradyzoite differentiation (rat embryonic brain cells) models confirmed TgCycP2 role in bradyzoite replication and revealed that stress induced TgCyc5 is critical for efficient tissue cyst maturation.

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mRNA-seq of immortailized bone marrow derived macrophages (iBMDM) infected with type II Toxoplasma gondii

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2019-03-25 | GSE128752 | GEO

Gasdermin-D-dependent IL-1 alpha release from microglia promotes protective immunity during chronic Toxoplasma gondii infection

Project description:Gasdermin-D-dependent IL-1 alpha release from microglia promotes protective immunity during chronic Toxoplasma gondii infection

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Anti-tumor Effect and Action Mechanism of Exosomes Derived from Toxoplasma gondii-Infected Dendritic Cells in Mice Colorectal Cancer

Project description:Toxoplasma gondii is an obligate intracellular protozoan with anti-tumor activity against a variety of cancers. However, the therapeutic effect of T. gondii on colorectal cancer is unclear, and using direct Toxoplasma infection in immunotherapy involves safety concerns. This study investigated the anti-tumor effect and mechanism of exosomes derived from dendritic cells (DC) infected with T. gondii (Me49-DC-Exo). We used the density gradient centrifugation to isolate exosomes from uninfected DCs (DC-Exo) and T. gondii Me49-infected DCs (Me49-DC-Exo). The isolated exosomes were identified by transmission electron microscopy, nanoparticle tracking analysis, and western blotting. Me49-DC-Exo significantly inhibited tumor growth and reduced the proportion of M2 macrophages in the blood of tumor-bearing mice. In vitro, Me49-DC-Exo suppressed macrophage (RAW264.7) polarization to M2 phenotype. miRNA sequencing revealed that multiple miRNAs in Me49-DC-Exo were differentially expressed compared with DC-Exo. miR-182-5p, miR-155-5p, miR-125b-2-3p, and miR-155-3p were up-regulated, while miR-9-5p was significantly down-regulated. Transfecting mimics or inhibitors of these differential miRNAs into RAW264.7 cells showed that miR-155-5p promoted M1 macrophage polarization while inhibiting M2 macrophage polarization. Bioinformatics prediction and dual-luciferase reporter assay confirmed the suppressor of cytokine signaling 1 (SOCS1) as a direct target of miR-155-5p. Silencing SOCS1 gene expression in RAW264.7 cells increased CD86 + CD206 - M1 macrophage proportion and inducible nitric oxide synthase and tumor necrosis factor-α mRNA levels. However, arginase1 and transglutaminase 2 expression levels decreased. These results suggest that the exosomes inhibit macrophage polarization to M2 phenotype and regulate SOCS1 expression by delivering functional miR-155-5p. These findings provide new ideas for colorectal cancer immunotherapy.

2022-02-24 | GSE197114 | GEO

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