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Molecular Pharmacology

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Research ArticleArticle

Rifampicin Is Not an Activator of the Glucocorticoid Receptor in A549 Human Alveolar Cells

Dany Jaffuel, Pascal Demoly, Claire Gougat, Gisèle Mautino, Jean Bousquet and Marc Mathieu
Molecular Pharmacology May 1999, 55 (5) 841-846;
Dany Jaffuel
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Pascal Demoly
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Claire Gougat
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Gisèle Mautino
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Jean Bousquet
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Marc Mathieu
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Abstract

It has recently been reported that rifampicin activates the glucocorticoid receptor and acts as an immunosuppressive drug. Because rifampicin constitutes an essential part of pulmonary tuberculosis therapy, we have examined whether it triggers glucocorticoid-like effects in alveolar cells. We have used reporter gene assays to measure the trans-activating and trans-repressing capacity of the glucocorticoid receptor after treating A549 human alveolar cells with rifampicin. The data show that rifampicin neither activated transcription from a promoter containing a glucocorticoid response element nor repressed the activity of activator protein 1 and nuclear factor κB, which are transcription factors involved in the immune response. In addition, rifampicin was also unable to inhibit the expression of an endogenous gene that contains activator protein 1 and nuclear factor κB response elements and encodes the proinflammatory cytokine RANTES (regulated upon activation normal T expressed and secreted protein). Finally, nuclear translocation of the glucocorticoid receptor, which occurs after ligand binding, was not triggered by rifampicin. In contrast, the glucocorticoid dexamethasone scored positive in all corresponding control experiments. In conclusion, rifampicin is not an activator of the glucocorticoid receptor in A549 alveolar cells. Our results support the clinical observation that rifampicin is not an immunosuppressive drug and suggest that the current medical practice concerning this antibiotic should not be changed.

Footnotes

  • Send reprint requests to: Dr. Pascal Demoly, Service des Maladies Respiratoires-INSERM U454, Hôpital Arnaud de Villeneuve, CHU de Montpellier, 34295 Montpellier Cedex 5, France. E-mail:demoly{at}montp.inserm.fr

  • G.M. is supported by a grant from the Conseil Régional du Languedoc-Roussillon and by a grant from the Ministère de la Recherche.

  • Abbreviations:
    RIF
    rifampicin
    GC
    glucocorticoid
    GRE
    glucocorticoid response element
    GR
    glucocorticoid receptor
    DEX
    dexamethasone
    AP-1
    activator protein 1
    NF-κB
    nuclear factor-κB
    RANTES
    regulated upon activation normal T expressed and secreted protein
    DTT
    dithiothreitol
    TNF-α
    tumor necrosis factor α
    TRE
    12-O-tetradecanoyl-phorbol-13-acetate response element
    NF-κBRE
    NF-κB response element
    • Received November 30, 1998.
    • Accepted January 25, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Molecular Pharmacology: 55 (5)
Molecular Pharmacology
Vol. 55, Issue 5
1 May 1999
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Research ArticleArticle

Rifampicin Is Not an Activator of the Glucocorticoid Receptor in A549 Human Alveolar Cells

Dany Jaffuel, Pascal Demoly, Claire Gougat, Gisèle Mautino, Jean Bousquet and Marc Mathieu
Molecular Pharmacology May 1, 1999, 55 (5) 841-846;

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Research ArticleArticle

Rifampicin Is Not an Activator of the Glucocorticoid Receptor in A549 Human Alveolar Cells

Dany Jaffuel, Pascal Demoly, Claire Gougat, Gisèle Mautino, Jean Bousquet and Marc Mathieu
Molecular Pharmacology May 1, 1999, 55 (5) 841-846;
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