Quorum sensing interference by phenolic compounds - A matter of bacterial misunderstanding

Over the past decade, numerous publications have emerged in the literature focusing on the in-hibition 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 con-centrations, and evaluated by which QS inhibition mechanisms they may act. The biotechno-logical 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.

Automated summary

In the past decade, there has been a significant amount of literature discussing the inhibition of quorum sensing (QS) by plant extracts and phenolic compounds. However, there is a lack of studies on the specific mechanisms behind these inhibitory effects. This study focuses on the most studied QS system, autoinducer type 1 (AI-1), and aims to understand the cellular level actions of phenolic compounds and the potential mechanisms of QS inhibition. The use of QS inhibitors in biotechnological applications holds promising prospects for the pharmaceutical and food industries as adjunct therapies and in preventing biofilms on various surfaces.