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Antimicrobial Agents and Chemotherapy, December 2007, p. 4225-4230, Vol. 51, No. 12
0066-4804/07/$08.00+0     doi:10.1128/AAC.00985-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Rifampin Inhibits Prostaglandin E2 Production and Arachidonic Acid Release in Human Alveolar Epithelial Cells{triangledown}

Yael Yuhas,1,3* Inbar Azoulay-Alfaguter,1,3 Eva Berent,1 and Shai Ashkenazi1,2,3

Laboratory of Infectious Diseases, Felsenstein Medical Research Center,1 Department of Pediatrics A, Schneider Children's Medical Center of Israel, Petach Tikva,2 Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel3

Received 29 July 2007/ Accepted 24 September 2007

Rifampin, a potent antimicrobial agent, is a major drug in the treatment of tuberculosis. There is evidence that rifampin also serves as an immunomodulator. Based on findings that arachidonic acid and its metabolites are involved in the pathogeneses of Mycobacterium tuberculosis infections, we investigated whether rifampin affects prostaglandin E2 (PGE2) production in human alveolar epithelial cells stimulated with interleukin-1ß. Rifampin caused a dose-dependent inhibition of PGE2 production. At doses of 100, 50, and 25 µg/ml, it inhibited PGE2 production by 75%, 59%, and 45%, respectively (P < 0.001). Regarding the mechanism involved, rifampin caused a time- and dose-dependent inhibition of arachidonic acid release from the alveolar cells. At doses of 100, 50, 25, and 10 µg/ml, it significantly inhibited the release of arachidonic acid by 93%, 64%, 58%, and 35%, respectively (P < 0.001). Rifampin did not affect the phosphorylation of cytosolic phospholipase A2 or the expression of cyclooxygenase-2. The inhibition of PGE2, and presumably other arachidonic acid products, probably contributes to the efficacy of rifampin in the treatment of tuberculosis and may explain some of its adverse effects.

* Corresponding author. Mailing address: Laboratory of Infectious Diseases, Felsenstein Medical Research Center, Beilinson Campus, Petach Tikva 49100, Israel. Phone: 972-3-9376736. Fax: 972-3-9253056. E-mail: yuhas{at}post.tau.ac.il

{triangledown} Published ahead of print on 1 October 2007.

Antimicrobial Agents and Chemotherapy, December 2007, p. 4225-4230, Vol. 51, No. 12
0066-4804/07/$08.00+0     doi:10.1128/AAC.00985-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Yuhas, Y., Berent, E., Cohen, R., Ashkenazi, S. (2009). Roles of NF-{kappa}B Activation and Peroxisome Proliferator-Activated Receptor Gamma Inhibition in the Effect of Rifampin on Inducible Nitric Oxide Synthase Transcription in Human Lung Epithelial Cells. Antimicrob. Agents Chemother. 53: 1539-1545 [Abstract] [Full Text]  


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