AbaI/AbaR Quorum Sensing in Acinetobacter baumannii: Virulence Regulation, Epithelial Injury, Innate Immune Activation and Anti-Virulence Strategies

Acinetobacter baumannii (A. baumannii) is an important cause of healthcare-associated infections due to its remarkable capacity for environmental persistence and multidrug resistance. The quorum-sensing (QS) network, particularly the AbaI/AbaR system, contributes to the regulation of several traits involved in colonization and infection. Current evidence indicates that AbaI/AbaR-mediated signalling coordinates biofilm formation, surface-associated motility, antimicrobial tolerance via modulation of efflux pump activity, oxidative stress responses and membrane integrity, as well as biofilm-associated antibiotic resistance and stress adaptation. QS also influences interactions with host cells, including epithelial damage and modulation of innate immune responses, although its role in adaptive immunity remains largely unresolved. This review summarises current knowledge of the molecular mechanisms underlying AbaI/AbaR-mediated signalling, its role in regulating A. baumannii infection-relevant phenotypes and host-pathogen interactions. It also discusses the therapeutic potential of quorum-quenching (QQ) strategies for attenuating A. baumannii virulence, as well as their current limitations in infection control.