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<p><i>Enterobacter</i> spp., members of the ESKAPE group of pathogens, are increasingly recognized for their involvement in nosocomial infections and remarkable adaptability, particularly in hospital settings. This review highlights the intricate quorum-sensing (QS) systems in Enterobacter species, emphasizing both canonical and non-canonical pathways, including the acyl-homoserine lactone–mediated AI-1 system, LuxS-dependent AI-2 systems, and the solo LuxR system. QS systems regulate critical bacterial behaviors, including biofilm formation, antibiotic resistance, and virulence gene expression. Additionally, the role of quorum quenching (QQ) as a potentially effective anti-virulence strategy is also discussed, with a focus on enzymatic and natural-product-based approaches that disrupt bacterial communication. Enzymes, such as lactonases, and synthetic or plant-derived QS inhibitors have been explored for their ability to attenuate pathogenic traits without exerting the selective pressure that typically drives antimicrobial resistance. Despite significant advances in elucidating QS and QQ processes in Enterobacter spp., notable limitations remain in the molecular understanding of species-specific QS control, particularly regarding the AI-3 signalling pathway and its functional significance. This extensive study seeks to promote future investigations into quorum-sensing disruption as a novel anti-virulence approach and its possible therapeutic application.</p>

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Quorum sensing disruption in Enterobacter spp.: unlocking new therapeutic pathways against multidrug-resistant infections

  • 期刊论文

  • 发表日期：

    2026年3月28日

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  • Kayeen Vadakkan,
  • Kavya Santhosh Ponnathodi,
  • Suriyakala Gunasekaran,
  • Sathiyaraj Sivaji,
  • Mariya Johnson,
  • Rini Raphael

摘要

Enterobacter spp., members of the ESKAPE group of pathogens, are increasingly recognized for their involvement in nosocomial infections and remarkable adaptability, particularly in hospital settings. This review highlights the intricate quorum-sensing (QS) systems in Enterobacter species, emphasizing both canonical and non-canonical pathways, including the acyl-homoserine lactone–mediated AI-1 system, LuxS-dependent AI-2 systems, and the solo LuxR system. QS systems regulate critical bacterial behaviors, including biofilm formation, antibiotic resistance, and virulence gene expression. Additionally, the role of quorum quenching (QQ) as a potentially effective anti-virulence strategy is also discussed, with a focus on enzymatic and natural-product-based approaches that disrupt bacterial communication. Enzymes, such as lactonases, and synthetic or plant-derived QS inhibitors have been explored for their ability to attenuate pathogenic traits without exerting the selective pressure that typically drives antimicrobial resistance. Despite significant advances in elucidating QS and QQ processes in Enterobacter spp., notable limitations remain in the molecular understanding of species-specific QS control, particularly regarding the AI-3 signalling pathway and its functional significance. This extensive study seeks to promote future investigations into quorum-sensing disruption as a novel anti-virulence approach and its possible therapeutic application.