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Antimicrobial Agents and Chemotherapy, April 2005, p. 1302-1305, Vol. 49, No. 4
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.4.1302-1305.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Glycerol Monolaurate Inhibits Virulence Factor Production in Bacillus anthracis

Sara M. Vetter and Patrick M. Schlievert*

Department of Microbiology, University of Minnesota Medical School, Minneapolis, Minnesota

Received 24 August 2004/ Returned for modification 1 December 2004/ Accepted 12 December 2004

Anthrax, caused by Bacillus anthracis, has been brought to the public's attention because of the 2001 bioterrorism attacks. However, anthrax is a disease that poses agricultural threats in the United States as well as human populations in Europe, China, Africa, and Australia. Glycerol monolaurate (GML) is a compound that has been shown to inhibit exotoxin production by Staphylococcus aureus and other gram-positive bacteria. Here, we study the effects of GML on growth and toxin production in B. anthracis. The Sterne strain of B. anthracis was grown to post-exponential phase with 0-, 10-, 15-, or 20-µg/ml concentrations of GML and then assayed quantitatively for protective antigen (PA) and lethal factor (LF). After 8 h, GML at concentrations greater than 20 µg/ml was bacteriostatic to growth of the organism. However, a 10-µg/ml concentration of GML was not growth inhibitory, but amounts of PA and LF made were greatly reduced. This effect was not global for all proteins when total secreted protein from culture fluids was examined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Through quantitative reverse transcription-PCR assays, this toxin-inhibitory effect was shown to occur at the transcriptional level, since amounts of mRNA for pagA (PA), lef (LF), and cya (edema factor) were reduced. Surprisingly, mRNA levels of atxA, a regulator of exotoxin gene expression, rose in the presence of GML. These data will be useful in developing therapeutic tools to treat anthrax disease, whether in animals or humans. These results also suggest that mechanisms of virulence regulation exist independent of atxA.

* Corresponding author. Mailing address: Department of Microbiology, University of Minnesota Medical School, MMC 196, 420 Delaware St., SE, Minneapolis, MN 55455. Phone: (612) 624-1484. Fax: (612) 626-0623. E-mail: pats{at}lenti.med.umn.edu.

Antimicrobial Agents and Chemotherapy, April 2005, p. 1302-1305, Vol. 49, No. 4
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.4.1302-1305.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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