Censored at the Nanoscale

As soon as researchers uncovered microorganisms’ abilities to communicate, efforts began to control the conversation. Among other cellular functions, quorum-sensing is implicated in biofilm formation, a problematic phenomena in a variety of settings such as persistence of infections (Costerton et al., 1999; Rutherford and Bassler, 2012) and biofouling of waterand wastewatertreatment membranes (Flemming, 1997; Ramesh et al., 2007; Yeon et al., 2008; Shrout and Nerenberg, 2012). Cell-to-cell communication has also been documented in biofilm dispersal leading to further propagation of biofilms within these systems (Solano et al., 2014). Many efforts to interrupt and quench quorum-sensing have exploited the knowledge of signaling systems using specific model organisms, most notably Pseudomona aeruginosa, Staphylococcus aureus, and Vibrio fischeri (Stevens and Greenberg, 1997; Miller and Bassler, 2001; Schuster and Greenberg, 2006; Novick and Geisinger, 2008). However, specific approaches have been developed to target and block gene-regulation or to inactivate receptor proteins, however, these approaches may have limited effects in mixed-community biofilms. Non-specific quenching of quorum-sensing molecules may have broader impact. Microbially-generated enzymes such as lactonases and acylases can hydrolyse N-acyl-L-homoserine lactones (HSLs), and interfere with communication (Park et al., 2006; Uroz et al., 2008; Romero et al., 2011). Both naturally-derived-, such as rosamaric acid and vanillin (Walker et al., 2004; Choo et al., 2006; Ponnusamy et al., 2009), and synthetic-chemicals, including brominated furanones, have been shown to effectively inhibit biofilm formation. The delivery of effective and non-toxic quorum-sensing inhibitors however, remains a challenge in managing biofilms. In a recent Frontiers in Microbiology article, Miller et al. (2015) introduce a different and unique approach that exploited the slightly-hydrophobic core of a beta-cyclodextrin (β-CD) to non-specifically bindHSLs, and quench the signaling between V. fischeri cells. What makes Miller et al.’s approach stand apart is they immobilized the β-CD on the surface of silicon dioxide nanoparticles1(Si-NPs). Like quorum-inhibition and quenching approaches, NPs, on their own, offer opportunities for biofilm control. NPs are being explored to inhibit or prevent biofilm formation on surfaces (Kalishwaralal et al., 2010; Tran and Webster, 2011) as well as increase biofilm vulnerability to antibiotics (Applerot et al., 2012; Radzig et al., 2013). Miller et al. have demonstrated a proofof-concept approach, using NPs for quorum-quenching. However, NP penetration into biofilms