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Staphylococcus epidermidis Polysaccharide Intercellular Adhesin Production Significantly Increases during Tricarboxylic Acid Cycle Stress

Cuong Vuong,¹ Joshua B. Kidder,^2, Erik R. Jacobson,³ Michael Otto,¹ Richard A. Proctor,^2,4 and Greg A. Somerville^1,5*

Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, Montana 59840,¹ Departments of Medical Microbiology and Immunology,² Medicine, University of Wisconsin Medical School, 1300 University Ave., Madison, Wisconsin 53706,⁴ University of Nebraska-Lincoln, Department of Biochemistry, Beadle Center, University of Nebraska, Lincoln, Nebraska 68588-0664,³ University of Nebraska-Lincoln, Department of Veterinary and Biomedical Sciences, 120 VBS Fair St., Lincoln, Nebraska 68583-0905⁵

Received 1 December 2004/ Accepted 25 January 2005

Staphylococcal polysaccharide intercellular adhesin (PIA) is important for the development of a mature biofilm. PIA production is increased during growth in a nutrient-replete or iron-limited medium and under conditions of low oxygen availability. Additionally, stress-inducing stimuli such as heat, ethanol, and high concentrations of salt increase the production of PIA. These same environmental conditions are known to repress tricarboxylic acid (TCA) cycle activity, leading us to hypothesize that altering TCA cycle activity would affect PIA production. Culturing Staphylococcus epidermidis with a low concentration of the TCA cycle inhibitor fluorocitrate dramatically increased PIA production without impairing glucose catabolism, the growth rate, or the growth yields. These data lead us to speculate that one mechanism by which staphylococci perceive external environmental change is through alterations in TCA cycle activity leading to changes in the intracellular levels of biosynthetic intermediates, ATP, or the redox status of the cell. These changes in the metabolic status of the bacteria result in the attenuation or augmentation of PIA production.

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