Quorum sensing gene abaI enhancing mucus production and pathogenicity of Acinetobacter baumannii

Background Acinetobacter baumannii (A. baumannii) is a gram-negative coccobacillus that can cause a variety of infectious diseases. In recent years, its high antibiotic resistance and lethality have posed great challenges to clinical treatment. The Quorum Sensing (QS) system is a widespread group behavior regulation mechanism in bacteria, which plays an important role in the virulence regulation of several gram-negative pathogenic bacteria.Methods In this study, a clinical mucus carbapenem-resistant Acinetobacter baumannii (CRAB110) was used to construct abaI knockout strain using CRISPR/Cas9 gene editing, and the abaI gene was complemented by the pYMAb2 plasmid. Then, the effects of abaI gene knockout on the capsule changes, virulence and host immunity were analyzed from the aspects of bacterial phenotype, physiology, molecules and the effects of bacteria on the host.Results The results showed CRAB110ΔabaI significantly affected capsule, virulence, and immunity compared to CRAB110, with smoother wall, thinner capsule, and lower virulence. CRAB110ΔabaI-induced inflammation was attenuated in mice. Transcriptome analysis revealed differential genes in polysaccharide synthesis (wza, wzb, wzc), galactose metabolism (GalM), ABC transport, and amino acid metabolism. Cellular Western-blot and mouse lung transcriptome suggested QS regulates A. baumannii-induced inflammation in mice via IL-17 and NF-κB pathways.Conclusions This study showed abaI gene boosts mucus production and pathogenicity of A. baumannii strains, providing new insights for clinical management of drug-resistant bacteria diseases and a foundation for new antimicrobial drugs.