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Bacterial quorum sensing pathways are complex communication systems that allow bacteria to monitor their population density and coordinate collective behaviors. This process relies on the production and detection of extracellular signaling molecules called autoinducers, such as acyl-homoserine lactones in Gram-negative bacteria and oligopeptides in Gram-positive bacteria (Miller & Bassler, 2001). When these signals reach a threshold concentration, they bind to cognate receptors, typically transcription factors, to trigger the expression of genes involved in virulence, biofilm formation, and antibiotic resistance (Rutherford & Bassler, 2012). Because these pathways are central to the pathogenicity of many clinical isolates, they are prime targets for anti-virulence strategies that aim to disarm pathogens rather than kill them (Defoirdt, 2018). Therapeutic intervention, often termed quorum quenching, involves using small molecules or enzymes to inhibit signal synthesis, degrade the signals, or block receptor binding (Hentzer et al., 2003). This approach is particularly promising for treating chronic infections, such as those found in cystic fibrosis or non-healing wounds, where biofilms protect bacteria from conventional antibiotics.
Inhibition of autoinducer synthesis, enzymatic degradation of signaling molecules (quorum quenching), and competitive antagonism of autoinducer receptors to prevent gene transcription.
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