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ISAba1-Mediated crp-osmC Amplification Enhances Host-Associated Fitness in Acinetobacter baumannii

ABSTRACT: Acinetobacter baumannii is a pathogen, highly adaptable to both hospital and host-associated environments. Understanding the genetic mechanisms underlying its adaptability is critical for controlling its persistence. Our study identified the crp-osmC gene cluster, flanked by ISAba1 elements, as a significant genetic structure undergoing amplification in A. baumannii. By experimentally mimicking the amplification of this gene cluster, we found that it substantially enhanced bacterial growth and competitiveness, while also increasing biofilm formation and serum resistance. Furthermore, amplification of the crp-osmC cluster enhanced colonization in murine infection models. Notably, this amplification was largely limited to the epidemic ST2 lineage clinical isolates. Intriguingly, gene amplification was also accompanied by heightened susceptibility to several antibiotics. Overall, ISAba1-mediated amplification of the crp-osmC cluster enhances host-associated fitness in A. baumannii, while the accompanying increase in antibiotic sensitivity reflects a trade-off between survival and resistance.

ORGANISM(S): Acinetobacter baumannii

PROVIDER: GSE331122 | GEO | 2026/05/20

REPOSITORIES: GEO

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Project description:Analysis of the effect of human pleural fluid on the transcriptome of Acinetobacter baumanii A118 Acinetobacter baumannii (Ab) is one of the most treacherous pathogens among those causing hospital-acquired pneumonia (HAP). A. baumannii possesses an adaptable physiology, seen not only in its antibiotic resistance and virulence phenotypes, but also in its metabolic versatility. In this study, we observed that A. baumannii undergoes global transcriptional changes in response to human pleural fluid (PF), a key host-derived environmental signal. Differential gene expression analyses combined with experimental approaches revealed changes in A. baumannii metabolism, affecting cytotoxicity, persistence, bacterial killing and chemotaxis. Over 55% of the differentially expressed transcriptomic genes corresponded to metabolic processes, including the up regulation of glutamate, short chain fatty acid, and styrene metabolism. We observed an up regulation of the pyruvate dehydrogenase complex and found that pyruvate (PYR), in conjunction with PF, triggers an A. baumannii pathogenic behavior that adversely impacts human epithelial cell viability. Interestingly, PF also amplified A. baumannii cytotoxicity against murine macrophages, suggesting an immune evasion strategy implemented by A. baumannii. Moreover, we uncovered opposing metabolic strategies dependent on the degree of pathogenicity of the strains, where less pathogenic strains demonstrated greater utilization of PYR to promote persister formation in the presence of PF. Additionally, our transcriptomic analysis and growth studies of A. baumannii suggest the existence of an alternative phenylalanine (PA) catabolic route independent of the phenylacetic acid pathway, which converts PA to phenylpyruvate (PP) and shuttles intermediates into styrene metabolism. This alternative route promoted a neutrophil-evasive state, as PF-induced degradation of PP significantly reduced overall human neutrophil chemotaxis in ex vivo chemotactic assays. Taken together, these data highlights A. baumannii pathoadaptabililty in response to host signals and provide further insight into the role of bacterial metabolism in virulence traits, antibiotic persistence strategies, and host innate immune evasion.

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ISAba1-Mediated crp-osmC Amplification Enhances Host-Associated Fitness in Acinetobacter baumannii

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