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Quorum sensing (QS) is a density-dependent chemical communication system used by bacteria to coordinate collective behaviors, including biofilm formation and virulence factor production [1, 2]. In biofilm-forming bacteria, QS pathways rely on the synthesis, secretion, and detection of signaling molecules called autoinducers, such as acyl-homoserine lactones (AHLs) in Gram-negative species and autoinducing peptides (AIPs) in Gram-positive species [6, 11]. When a threshold concentration of these signals is reached, they bind to cognate receptors to trigger large-scale changes in gene expression that facilitate the transition from a planktonic to a sessile, biofilm-protected state [3, 5]. This process is a critical driver of chronic infections and antibiotic tolerance, as biofilms shield bacteria from host immune responses and antimicrobial agents [8, 13]. Therapeutic strategies targeting QS, known as quorum quenching, aim to attenuate bacterial pathogenicity without imposing the strong selective pressure for resistance associated with traditional bactericidal antibiotics [4, 15].
Inhibition of autoinducer synthesis, enzymatic degradation of autoinducers (quorum quenching), competitive antagonism of autoinducer receptors, and disruption of downstream signal transduction cascades [1, 11, 15].
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