Enhancement of In Vitro hsp72 Expression by Placental IL-6

Authors

  • S. MIRANDA,

    1. Instituto de Estudios de la Inmunidad Humoral (IDEHU), CONICET-UBA, Facultad de Farmacia y Bioquímica de la Universidad de Buenos Aires, Buenos Aires, Argentina
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  • T. GENTILE,

    1. Instituto de Estudios de la Inmunidad Humoral (IDEHU), CONICET-UBA, Facultad de Farmacia y Bioquímica de la Universidad de Buenos Aires, Buenos Aires, Argentina
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  • R. MARGNI

    1. Instituto de Estudios de la Inmunidad Humoral (IDEHU), CONICET-UBA, Facultad de Farmacia y Bioquímica de la Universidad de Buenos Aires, Buenos Aires, Argentina
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Address reprint requests to: S. Miranda, Instituto de Estudios de la Inmunidad Humoral (IDEHU), CONICET-UBA, Facultad de Farmacia y Bioquímica de la Universidad de Buenos Aires, Junín 956 4P (1113), Buenos Aires, Argentina.

E-mail: SMiranda@ffyb.uba.ar

Abstract

PROBLEM: To give an approach in order to elucidate the mechanism by which placental IL-6 induce modifications in the glycosylation status of immunoglobulins, in the present work, we investigate a putative relationship between a stimulus by placental IL-6 and expression of cytoplasmic “hsp70 family proteins” in an in vitro model.
METHODS OF STUDY: Supernatants of cultures of placentae obtained from primiparous and multiparous AKR/J×AKR/J and AKR/J×BALB/c mouse crossbreedings were added to mouse IgG1 hybridoma cultures which produced symmetric and asymmetric anti-dinitrophenol (anti-DNP) antibodies. Analyses of the expression of inducible hsp72/constitutive hsp73 in cellular lysates obtained from hybridomas cultured, in the presence of rmIL-6 or crude murine placental culture supernatants, followed by neutralization assays with anti IL-6, were performed. In addition, the level of IL-6 present in the employed placental culture supernatants was determined and compared with the placental hsp70-inducing effect.
RESULTS: These experiments showed that mouse placentae were able to release IL-6 in vitro. In addition, mouse placental supernatants (PS) containing over 1,000 pg/mL of IL-6 enhanced the expression of the inducible isoform hsp72 in the employed hybridomas. This effect was abolished when the hsp70-inducing PS were previously incubated with anti-mIL6 antibody.
CONCLUSIONS: These observations indicate that mouse placentae produce different titers of IL-6 and suggest that IL-6 appears to be the unique mouse placental factor able to induce in vitro hsp72 synthesis. A relationship with the increased synthesis of anti-paternal antigen asymmetric antibodies, previously observed during pregnancy, is discussed.

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