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Vol. 55, Issue 5, 841-846, May 1999
Institut National de la Santé et de la Recherche
Médicale U454 and the Service des Maladies Respiratoires, CHU de
Montpellier, Montpellier, France.
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 
B, 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 B 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.
This article has been cited by other articles:
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  Y. Yuhas, I. Azoulay-Alfaguter, E. Berent, and S. Ashkenazi Rifampin Inhibits Prostaglandin E2 Production and Arachidonic Acid Release in Human Alveolar Epithelial Cells Antimicrob. Agents Chemother., December 1, 2007; 51(12): 4225 - 4230. [Abstract] [Full Text] [PDF]
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 J. Rosen and J. N. Miner The Search for Safer Glucocorticoid Receptor Ligands Endocr. Rev., May 1, 2005; 26(3): 452 - 464. [Abstract] [Full Text] [PDF]
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 R. Nau and H. Eiffert Modulation of Release of Proinflammatory Bacterial Compounds by Antibacterials: Potential Impact on Course of Inflammation and Outcome in Sepsis and Meningitis Clin. Microbiol. Rev., January 1, 2002; 15(1): 95 - 110. [Abstract] [Full Text] [PDF]
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 J. Visser, J. L. Hillebrands, and J. Rozing No evidence that rifampicin has glucocorticoid-like immunosuppressive properties leading to suppression of rat-splenocyte proliferation in vitro J. Antimicrob. Chemother., June 1, 2001; 47(6): 894 - 895. [Full Text] [PDF]
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 A. S. Herr, G. M. Wochnik, M. C. Rosenhagen, F. Holsboer, and T. Rein Rifampicin Is Not an Activator of Glucocorticoid Receptor Mol. Pharmacol., April 1, 2000; 57(4): 732 - 737. [Abstract] [Full Text]
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 E. G. Schuetz, W. Schmid, G. Schutz, C. Brimer, K. Yasuda, T. Kamataki, L. Bornheim, K. Myles, and T. J. Cole The Glucocorticoid Receptor Is Essential for Induction of Cytochrome P-4502B by Steroids but Not for Drug or Steroid Induction of CYP3A or P-450 Reductase in Mouse Liver Drug Metab. Dispos., March 1, 2000; 28(3): 268 - 278. [Abstract] [Full Text] [PDF]
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B. Goodwin, E. Hodgson, and C. Liddle The Orphan Human Pregnane X Receptor Mediates the Transcriptional Activation of CYP3A4 by Rifampicin through a Distal Enhancer Module Mol. Pharmacol., December 1, 1999; 56(6): 1329 - 1339. [Abstract] [Full Text]
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