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[Toxoplasma gondii Rhoptry Protein 17 Inhibits the Apoptosis of Mouse Macrophages via Activation of Activator Protein

Hai-long Wang, Jia-xin Xing, Shan Guo

    Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi = Chinese Journal of Parasitology & Parasitic Diseases
    |August 25, 2018
    PubMed
    Abstract

    Insights

    Toxoplasma gondii ROP17 protein inhibits apoptosis in macrophages, a process dependent on c-Jun phosphorylation and Bcl-3 expression. This finding offers insights into parasite-host interactions and cell death pathways.

    Area of Science:

    • Immunology
    • Cell Biology
    • Parasitology

    Background:

    • Toxoplasma gondii is an intracellular parasite that manipulates host cell functions.
    • Gamma-interferon (IFN-γ) is crucial for macrophage activation and defense against pathogens.
    • Apoptosis, or programmed cell death, is a key mechanism in host defense.

    Purpose of the Study:

    • To investigate the role of Toxoplasma gondii rhoptry protein 17 (ROP17) in regulating IFN-γ-induced apoptosis of mouse macrophages.
    • To elucidate the molecular mechanisms by which ROP17 influences macrophage cell death.

    Main Methods:

    • J774A.1 monocyte macrophages were transfected with ROP17-expressing or control plasmids.
    • Cells were treated with IFN-γ to induce apoptosis.
    • Flow cytometry and Western blotting were used to assess apoptosis rates and protein levels (phosphorylated c-Jun, cleaved Caspase-3, Bcl-2, Bcl-xL, Bcl-3).
    • RNA interference was employed to inhibit c-Jun expression and phosphorylation.

    Main Results:

    • Overexpression of ROP17 significantly reduced the apoptosis rate in IFN-γ-treated macrophages.
    • ROP17 overexpression led to increased levels of phosphorylated c-Jun and Bcl-3, and decreased levels of cleaved Caspase-3.
    • Bcl-2 and Bcl-xL levels were not significantly affected by ROP17.
    • Inhibition of c-Jun phosphorylation reversed the anti-apoptotic effect of ROP17 and reduced Bcl-3 expression.

    Conclusions:

    • Toxoplasma gondii ROP17 exhibits an anti-apoptotic effect on macrophages.
    • This anti-apoptotic function is mediated through the modulation of c-Jun phosphorylation and subsequent regulation of Bcl-3 expression.

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