Planta Med 2011; 77 - P_33
DOI: 10.1055/s-0031-1273562

Staphylococcus aureus Biofilm Inhibition by a Phenolic Glycoside-rich Extract of Rubus ulmifolius

CL Quave 1, C Compadre 2, H Hendrickson 2, K Beenken 1, MS Smeltzer 1, 3
  • 1Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205
  • 2Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205
  • 3Department of Orthopaedic Surgery and Center for Orthopaedic Research, University of Arkansas for Medical Sciences, Little Rock, AR 72205

Biofilm formation not only contributes to the pathogenesis of many forms of Staphylococcus aureus infection but also compromises antimicrobial therapy to a point that often necessitates surgical intervention. This makes it important to develop therapeutic approaches that can be used to limit biofilm formation to a therapeutically-relevant degree. A root extract from the elmleaf blackberry (Rubus ulmifolius Schott.) was created following bioassay-guided fractionation techniques and investigated for its ability to inhibit S. aureus biofilm formation. Active fractions were characterized by liquid chromatography time of flight mass spectrometry (LC-Q/ToFMS) to obtain a chromatographic fingerprint for batch-to-batch extract standardization. The elmleaf blackberry is a medicinal plant used in traditional medical treatments for skin and soft tissue infection in the Mediterranean [1]. Investigation of this extract revealed that it is effective in preventing biofilm formation in all of the genotypic variants of S. aureus, including the USA300 clonal lineage, at a minimum concentration of 50µg/mL. Moreover, concomitant treatment with the extract and antibiotic revealed that the extract improves the efficacy of functionally-distinct antibiotics in the specific context of treating an established S. aureus biofilm in a catheter model. Our findings provide support for the further characterization and investigation of this extract as a biofilm inhibitor.

Acknowledgements: This work was supported by the National Institutes of Health (F32AT005040 to C.L.Q. and R01-AI43356 to M.S.S.). The content is solely the responsibility of the authors and does not necessarily reflect the official views of the National Center for Complementary and Alternative Medicine or the National Institute of Allergy and Infectious Diseases at the National Institutes of Health.

References: [1] Quave C, Pieroni A, Bennett BC (2008) Journal of Ethnobiology and Ethnomedicine 4: 5.