Transcriptome data of Acinetobacter baumannii ATCC17978 and quorum sensing gene abaI mutants with or without sub MIC meropenem treatment.

Acinetobacter baumannii is a formidable pathogen renowned for its role in hospital acquired infections. In recent years, largely due to antibiotic abuse and other reasons, bacteria are frequently exposed to sub minimum inhibitory concentration (sub MIC) levels of antibiotics. Accumulating evidence suggests that sub MIC antibiotic pressure serves as a critical driver of bacterial resistance evolution and virulence adaptation. The quorum sensing (QS) system is a key bacterial signaling network that senses population density and coordinates vital physiological functions and environmental adaptations. Targeting QS system to attenuate virulence and resistance represents a promising strategy for combating multi drug resistant infections. Nevertheless, the role of systems in regulating antibiotic stress response in Acinetobacter baumannii has not been elucidated. We compared the wild type strain of Acinetobacter baumannii ATCC17978 and the isogenic abaI deletion mutant strain to investigate the expression profile of QS under sub MIC meropenem treatment. The analysis showed that, sub MIC meropenem triggered extensive gene expression changes in both the wild type and abaI deletion mutant strains. In the WT, differentially expressed genes were enriched in pathways including quorum sensing, biofilm formation, ABC transporters, and two component systems. In contrast, the abaI deletion mutant exhibited distinct transcriptional profiles, with enrichment in beta lactam resistance, aromatic amino acid biosynthesis, and metabolite transport.