Dexamethasone has pro-apoptotic effects on non-activated fresh peripheral blood mononuclear cells

Authors

  • Paulo Renato Rivas Totino,

    1. Department of Immunology, WHO Collaborating Center for Research and Training in the Immunology of Parasitic Diseases, Instituto Oswaldo Cruz, Fiocruz, RJ, Brazil
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  • Evelyn Kety Pratt Riccio,

    1. Department of Immunology, WHO Collaborating Center for Research and Training in the Immunology of Parasitic Diseases, Instituto Oswaldo Cruz, Fiocruz, RJ, Brazil
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  • Suzana Corte-Real,

    1. Department of Ultrastructure and Cellular Biology, Instituto Oswaldo Cruz, Fiocruz, RJ, Brazil
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  • Cláudio Tadeu Daniel-Ribeiro,

    1. Department of Immunology, WHO Collaborating Center for Research and Training in the Immunology of Parasitic Diseases, Instituto Oswaldo Cruz, Fiocruz, RJ, Brazil
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  • Maria de Fátima Ferreira-da-Cruz

    Corresponding author
    1. Department of Immunology, WHO Collaborating Center for Research and Training in the Immunology of Parasitic Diseases, Instituto Oswaldo Cruz, Fiocruz, RJ, Brazil
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Corresponding author. Instituto Oswaldo Cruz, Fiocruz, Pavilhão Leônidas Deane, Laboratório de Pesquisas em Malária. Av. Brasil, 4365, Manguinhos. Rio de Janeiro, RJ, Brasil, CEP: 21045-900. Tel.: +55 21 3865 8185; fax: +55 21 3865 8145. mffcruz@ioc.fiocruz.br

Abstract

Apoptosis is a physiological method of cell death commonly referred to as programmed cell death. However, non-apoptotic programmed cell death, such as autophagy and programmed necrosis, has been characterized by morphological criteria. In view of the human therapeutic use of DEX, and considering that no difference in the number and/or affinity of glucocorticoid receptors in activated and non-activated lymphocytes has been reported, we decided to evaluate the effect of DEX on fresh peripheral blood mononuclear cells (PBMC). Transmission electron microscopy showed that DEX can significantly induce apoptosis in non-activated PBMC. It was also observed by transmission electron microscopy that, independently of DEX treatment, PBMC also died by a process marked by extreme vacuolization and increase in cellular volume; these cells were erroneously classified as viable by flow cytometry using the 7-AAD assay. It is concluded that the DEX pro-apoptotic effect is not restricted to activated PBMC and, therefore, DEX-induced apoptosis could play either homeostatic (activated PBMC) or immunosuppressive (non-activated PBMC) roles.

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