Ochratoxin A mediates MAPK activation, modulates IL-2 and TNF-α mRNA expression and induces apoptosis by mitochondria-dependent and mitochondria-independent pathways in human H9 T cells

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  • Darif Youssef
    Laboratory of Physiology and Molecular Genetics, Immunology Unit, Faculty of Sciences, Hassan II Ain Chock University, Morocco
  • Mountassif Driss
    Department of Anatomy and Cell Biology, McGill University, Canada
  • Belkebir Abdelkarim
    Laboratory of Physiology and Molecular Genetics, Immunology Unit, Faculty of Sciences, Hassan II Ain Chock University, Morocco
  • Zaid Younes
    Laboratory of Thrombosis and Hemostasis, Montreal Heart Institute, Canada
  • Basu Kaustuv
    Department of Anatomy and Cell Biology, McGill University, Canada
  • Mourad Walid
    Laboratoire d’immunologie cellulaire et moléculaire, Centre de Recherche-Centre Hospitalier de l’Université de Montréal (CR-CHUM), Canada
  • Oudghiri Mounia
    Laboratory of Physiology and Molecular Genetics, Immunology Unit, Faculty of Sciences, Hassan II Ain Chock University, Morocco

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  • Ochratoxin A mediates MAPK activation, modulates <i>IL-2</i> and <i>TNF-α</i> mRNA expression and induces apoptosis by mitochondria-dependent and mitochondria-independent pathways in human H9 T cells

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Ochratoxin A (OTA) is a natural fungal secondary metabolite that contaminates food and animal feed. Human exposure and involvement of this mycotoxin in several pathologies have been demonstrated worldwide. We investigated OTA immunotoxicity on H9 cells, a human cutaneous CD4+ T lymphoma cell line. Cells were treated with 0, 1, 5, 10, and 20 µM OTA for up to 24 hr. Western blotting revealed increased phosphorylation of all three major mitogen-activated protein kinases (extracellular signal–regulated kinase, c-Jun amino-terminal kinase, p38). OTA triggered mitochondrial transmembrane potential loss and caspase-3 activation. The 24-hr OTA treatment caused marked changes in cell morphology and DNA fragmentation, suggesting the occurrence of apoptotic events that involved a mitochondria-dependent pathway. Moreover, OTA triggered significant modulation of survivin, interleukin 2 (IL-2) and tumor necrosis factor α (TNF-α): mRNA expression of survivin and IL-2 were decreased, while TNF-α was increased. OTA also caused caspase-8 activation in a time-dependent manner, which evokes the death receptor pathway activation; we suspect that this occurred via the autocrine pro-apoptotic effect of TNF-α on H9 cells.

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