Quorum sensing is a regulatory process used by bacteria for controlling gene expression in response to increasing cell density.¹ This regulatory process manifests itself with a variety of phenotypes including biofilm formation and virulence factor production.² Coordinated gene expression is achieved by the production, release, and detection of small diffusible signal molecules called autoinducers. The N-acylated homoserine lactones (AHLs) comprise one such class of autoinducers, each of which generally consists of a fatty acid coupled with homoserine lactone (HSL). AHLs vary in acyl group length (C₄-C₁₈), in the substitution of C3 (hydrogen, hydroxyl, or oxo group) and in the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signal specificity through the affinity of transcriptional regulators of the LuxR family.³ C18:1-Δ⁹ cis-(L)-HSL is a long-chain AHL that may have antimicrobial activity⁴ and thus, might be used to inhibit pathogenesis by regulating bacerial quorum sensing signaling.⁵

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