Nanoporous Superhydrophobic Coatings that Promote the Extended Release of Water-Labile Quorum Sensing Inhibitors and Enable Long-Term Modulation of Quorum Sensing in Staphylococcus aureus.

"The authors declare no competing financial interest."

"Financial support for this work was provided by the Office of Naval Research (N00014-07-1-0255). M.J.K. was supported, in part, by a Morgridge Wisconsin Distinguished Graduate Fellowship. T.Y. was supported, in part, by the UW–Madison NIH Biotechnology Training Program (T32 GM08349). The authors acknowledge use of instrumentation supported by the National Science Foundation through grants provided to the UW–Madison Materials Research Science and Engineering Center (MRSEC; DMR-1121288) and the UW–Madison Nanoscale Research and Engineering Center (NSEC; DMR-0832760). We gratefully acknowledge Professor Alexander R. Horswill for donation of the S. aureus AH1747 strain, Professor Richard Novick for donation of the RN6390B strain, Matthew C. D. Carter for technical assistance with release experiments, Dr. Uttam Manna for many helpful discussions, and Huong T. Kratochvil for assistance with graphics and illustrations. Using the S. aureus GFP reporter strain assay to monitor peptide activity, we observed the in situ release of peptide 1 to limit the production of GFP (and thereby agr-type QS) to less than 10% (relative to control coatings without loaded peptide) through the first 28 days of these experiments (representative results are shown in A; see for details of assay protocol). Optical density measurements performed as part of these GFP assays revealed that these reductions in fluorescence did not arise from bacterial cell death (Figure S3). Characterization of samples at later time points (e.g., days 42 and 56) revealed that GFP production began to increase but was still lower than that observed for untreated controls (all values from days 1 through 42 were statistically significant (p < 0.05)). This experiment was discontinued after day 56 because visual inspection revealed signs of film delamination and cracking at these longer time points. This behavior was similar to that observed during experiments to characterize release profiles (discussed above) but occurred much earlier in these experiments, presumably due to the additional repetitive washing and media changes required by these bacterial assays. We attribute the decrease in inhibition of GFP production at 42 and 56 days to result, at least in part (see discussion below), from these physical changes. Support for this view is provided by the results of otherwise identical experiments in which film delamination was not observed; production of GFP remained low for up to 56 days in those experiments (Figure S2A)."