Frontiers in microbiology · 2026
Quorum sensing gene abaI enhancing capsule production and pathogenicity of Acinetobacter baumannii.
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Qiu Zhilang, Zheng Yu, Yuan Kexin, Zhao Peiling, Wu Guanfeng, Zeng Yang, Cao Huijun, Zhao Xuejun, Hong Liang, Guo Guo, Mo Fei, Wang Yuping, Peng Jian
Аннотация
INTRODUCTION: Acinetobacter baumannii (A. baumannii) is a Gram-negative coccobacillus that can cause a variety of infectious diseases. The Quorum Sensing (QS) system is a widespread mechanism regulating group behavior in bacteria, playing a crucial role in the virulence regulation of several Gram-negative pathogenic bacteria. The aim of this study was to investigate the effects of the A. baumannii quorum sensing system on capsule production and pathogenicity.
METHODS: In this work, a clinical carbapenem-resistant A. baumannii with mucoid colonies (CRAB110) was used to construct an abaI knockout strain (CRAB110ΔabaI) using CRISPR/Cas9 system. Afterwards, changes in capsule production, bacterial virulence, and host immune responses were evaluated by assessing bacterial phenotypes, physiology, gene expression, and effects on the host.
RESULTS: The results showed that CRAB110ΔabaI significantly affected capsule production, virulence, and immunity compared with CRAB110. Mice infected with CRAB110ΔabaI exhibited a reduction in inflammation compared to those infected with CRAB110. A comparison of the transcriptomes of CRAB110 and CRAB110ΔabaI identified differentially expressed genes related to polysaccharide synthesis (wza, wzb, wzc), galactose metabolism (GalM), ABC transport, and amino acid metabolism. Mouse lung transcriptomic and cellular Western blot data indicated that quorum sensing (QS) exerts its pro-inflammatory effect through Acinetobacter baumannii by influencing the IL-17 and NF-κB pathways.
CONCLUSION: This study suggests that the abaI gene boosts capsule production and pathogenicity of A. baumannii, providing new insights for clinical management of drug-resistant A. baumannii diseases and a foundation for new antimicrobial drugs.
METHODS: In this work, a clinical carbapenem-resistant A. baumannii with mucoid colonies (CRAB110) was used to construct an abaI knockout strain (CRAB110ΔabaI) using CRISPR/Cas9 system. Afterwards, changes in capsule production, bacterial virulence, and host immune responses were evaluated by assessing bacterial phenotypes, physiology, gene expression, and effects on the host.
RESULTS: The results showed that CRAB110ΔabaI significantly affected capsule production, virulence, and immunity compared with CRAB110. Mice infected with CRAB110ΔabaI exhibited a reduction in inflammation compared to those infected with CRAB110. A comparison of the transcriptomes of CRAB110 and CRAB110ΔabaI identified differentially expressed genes related to polysaccharide synthesis (wza, wzb, wzc), galactose metabolism (GalM), ABC transport, and amino acid metabolism. Mouse lung transcriptomic and cellular Western blot data indicated that quorum sensing (QS) exerts its pro-inflammatory effect through Acinetobacter baumannii by influencing the IL-17 and NF-κB pathways.
CONCLUSION: This study suggests that the abaI gene boosts capsule production and pathogenicity of A. baumannii, providing new insights for clinical management of drug-resistant A. baumannii diseases and a foundation for new antimicrobial drugs.