Abstract
Biofilms are complex communities of microorganisms in organized structures attached to surfaces. Importantly, biofilms are a major cause of bacterial infections in humans, and remain one of the most significant challenges to modern medical practice. Unfortunately, conventional therapies have shown to be inadequate in the treatment of most chronic biofilm infections based on the extraordinary innate tolerance of biofilms to antibiotics. Antagonists of quorum sensing signaling molecules have been used as means to control biofilms. QS and other cell-cell communication molecules are able to revert biofilm tolerance, prevent biofilm formation and disrupt fully developed biofilms, albeit with restricted effectiveness. Recently however, it has been demonstrated that Pseudomonas aeruginosa produces a small messenger molecule cis-2-decenoic acid (cis-DA) that shows significant promise as an effective adjunctive to antimicrobial treatment of biofilms. This molecule is responsible for induction of the native biofilm dispersion response in a range of Gram-negative and Gram-positive bacteria and in yeast, and has been shown to reverse persistence, increase microbial metabolic activity and significantly enhance the cidal effects of conventional antimicrobial agents. In this manuscript, the use of cis-2-decenoic acid as a novel agent for biofilm control is discussed. Stimulating the biofilm dispersion response as a novel antimicrobial strategy holds significant promise for enhanced treatment of infections and in the prevention of biofilm formation.
Highlights
Biofilms are dynamic communities of closely associated microbial cells embedded within a hydrated extracellular polymeric substance (EPS) on an air-liquid interface, or adherent to inert or living surfaces and constitute the major proportion of bacterial biomass in nature [1]
Continuous exposure of P. aeruginosa PAO1 expressing green fluorescent protein (GFP), in flow cell reactors to Electric Power Research Institute (EPRI) medium supplemented with 1 nM, 1 μM or 1 mM of cis-2-decenoic acid (cis-DA) (Figure 1B–D, Table 2) under the conditions described by Davies and Marques [19], resulted in a significant reduction of maximum biofilm thickness (2-fold), average biofilm thickness (2.2, 1.4- and 8-fold lower, respectively), roughness coefficient (1.5-fold lower, 6.4-fold lower and no-fold change, respectively), and total biomass (2.4, 1.7- and 8.5-fold lower respectively), when compared to the absence of cis-DA (Figure 1, Table 2)
During the past 15 years, efforts to develop new and effective anti-biofilm chemotherapeutics has focused to a large degree on blocking the mechanism of signal transduction involved in cell-to-cell communication via quorum sensing, and has led to the development of several QS antagonists
Summary
Biofilms are dynamic communities of closely associated microbial cells embedded within a hydrated extracellular polymeric substance (EPS) on an air-liquid interface, or adherent to inert (abiotic) or living surfaces and constitute the major proportion of bacterial biomass in nature [1]. While there are numerous ongoing efforts to address the biofilm problem, the most promising strategies include those aimed at manipulating the mode of growth, by either preventing biofilms from forming, or by disrupting existing biofilms This is further supported by the finding that dispersion, the evacuation of bacterial cells from the biofilm, coincides with the reinstatement of antibiotic sensitivity [53,54,55]; suggesting that the potential to overcome the biofilm resistance mechanisms or to induce the transition of biofilm bacteria from a resistant to a susceptible phenotype would likely result in enhanced treatment options in fighting biofilm infections. This strategy takes advantage of the regulatory networks that are controlled by inter and intra-species signaling and will focus primarily upon the cross-kingdom signaling molecule cis-2-decenoic acid, a fatty acid signal that has been shown to prevent biofilm development, induce biofilm dispersion, cause global changes in cellular phenotype, modulate bacterial virulence and override microbial persistence
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