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Quorum sensing (QS) pathways in pathogenic poultry gut bacteria are sophisticated intercellular communication systems that regulate the expression of virulence factors, biofilm formation, and metabolic adaptation in response to cell population density. Key pathogens such as Salmonella enterica, Campylobacter jejuni, and Clostridium perfringens utilize these pathways—specifically the LuxS/AI-2 system, Acyl-homoserine lactone (AHL) signaling, and Autoinducing Peptide (AIP) systems—to synchronize the production of toxins and colonization factors (Frontiers in Microbiology, 2020; Veterinary Research, 2019). Because QS is central to the transition from a commensal-like state to a pathogenic state, it is a high-priority target for quorum quenching (QQ) interventions. These interventions aim to disrupt signal synthesis, degrade signaling molecules, or block receptor binding, thereby attenuating virulence without exerting the high selective pressure associated with traditional bactericidal antibiotics (Microorganisms, 2021). Current therapeutic candidates include plant-derived compounds like cinnamaldehyde and carvacrol, as well as specialized enzymes like AHL-lactonases, which have shown efficacy in reducing the impact of necrotic enteritis and salmonellosis in poultry models (Antibiotics, 2022).
Inhibition of autoinducer synthesis (e.g., LuxS inhibition), enzymatic degradation of signaling molecules (quorum quenching), and competitive antagonism of signal receptors (e.g., LuxR-type receptors).
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