The abaI/abaR quorum sensing system effects pathogenicity in Acinetobacter baumannii

Abstract

Acinetobacter baumannii is a Gram-negative pathogen that has emerged as one of the most troublesome pathogens for health care institutions globally. Bacterial quorum sensing (QS) is a process of cell-to-cell communication that relies on the production, secretion and detection of autoinducer (AI) signals to share information about cell density and regulate gene expression accordingly. In this study, we performed a comprehensive set of experiments show that deletion of quorum sensing genes showed differences in growth characteristics, morphology, biofilm formation and virulence, and increased susceptibility to some antimicrobials and exhibited motility defects. RNA-seq analysis indicated that genes involved in various aspects of energy production and conversion, Valine, leucine and isoleucine degradation and lipid transport and metabolism showed different expression. IMPORTANCEPrevious studies on bacterial quorum sensing mainly focused on biofilm formation and motility and antibiotic resistance. In this study, we focused on detecting the role of the abaI/abaR QS system in the virulence of A. baumannii. Our work provides a new insight into abaI/abaR quorum sensing system effects pathogenicity in A. baumannii. We propose that targeting the AHL synthase enzyme abaI could provide an effective strategy for attenuating virulence. On the contrary, interdicting the autoinducer synthase-receptor abaR elicits unpredictable consequences, which may lead to enhanced bacterial virulence.