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.

Acinetobacter baumannii (A. baumannii) is a major nosocomial pathogen that poses a significant threat to global health owing to its remarkable capacity for antimicrobial resistance, environmental persistence, and virulence. These adaptive traits are closely associated with its quorum-sensing (QS) network, particularly the AbaI/AbaR system. 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, thereby enhancing bacterial survival and fitness. Furthermore, QS signalling contributes to epithelial cell injury and to the modulation of innate immune responses during infection, whereas its effects on adaptive immunity remain poorly understood. 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, as well as the therapeutic potential of quorum quenching (QQ) strategies in attenuating A. baumannii virulence, while highlighting key knowledge gaps that warrant further mechanistic and translational investigation.