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Bacterial quorum-sensing (QS) and biofilm-associated genes constitute a complex regulatory network that enables bacteria to coordinate collective behaviors based on population density [7, 11]. This communication system relies on the production and detection of signaling molecules called autoinducers, such as N-acyl homoserine lactones (AHLs) in Gram-negative bacteria and autoinducing peptides (AIPs) in Gram-positive species [7, 9]. These genes regulate the transition from a nomadic planktonic state to a biofilm—a resilient, multicellular community encased in an extracellular matrix that protects bacteria from antibiotics and the host immune system [4, 6, 23]. Because QS and biofilm formation are central to the pathogenesis of chronic and healthcare-associated infections, they have emerged as promising targets for anti-virulence therapies [1, 17]. Drugs targeting these systems, such as quorum-sensing inhibitors (QSIs) and quorum-quenching (QQ) enzymes, aim to disrupt bacterial communication and biofilm integrity without necessarily killing the bacteria, thereby potentially reducing the selective pressure for resistance [1, 2, 12]. Clinical applications focus on treating persistent infections like those found in cystic fibrosis, chronic wounds, and on medical implants where traditional antibiotics often fail [4, 5, 21].
Inhibition of autoinducer synthesis, enzymatic degradation of signaling molecules (quorum quenching), antagonism of autoinducer receptors, and inhibition of downstream transcriptional regulators.
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