Abstract
Over the past decade, numerous publications have emerged in the literature focusing on the inhibition of quorum sensing (QS) by plant extracts and phenolic compounds. However, there is still a scarcity of studies that delve into the specific mechanisms by which these compounds inhibit QS. Thus, our question is whether phenolic compounds can inhibit QS in a specific or indirect manner and to elucidate the underlying mechanisms involved. This study is focused on the most studied QS system, namely, autoinducer type 1 (AI-1), represented by N-acyl-homoserine lactone (AHL) signals and the AHL-mediated QS responses. Here, we analyzed the recent literature in order to understand how phenolic compounds act at the cellular level, at sub-inhibitory concentrations, and evaluated by which QS inhibition mechanisms they may act. The biotechnological application of QS inhibitors holds promising prospects for the pharmaceutical and food industries, serving as adjunct therapies and in the prevention of biofilms on various surfaces.