Dataset Information

Nerol as an Anti-quorum sensing and Therapeutic Agent against Acinetobacter baumannii Pneumonia

ABSTRACT: Nerol subinhibitory concentrations block A. baumannii quorum sensing, inhibiting AHL, biofilm formation, motility, and EPS production. Proteomics validated these phenotypes, showing synchronous downregulation of key virulence proteins including BfmS and MacB. ITC confirmed its binding to BfmS disrupts the BfmRS two-component system. In a mouse pneumonia model, it significantly reduced lung bacterial load, blocked the NF-κB/MAPK axis, decreased inflammatory expression, restored lung tissue structure, and showed no hepatotoxicity. This provides a safe, non-antibiotic strategy for treating carbapenem-resistant Acinetobacter baumannii pneumonia.

ORGANISM(S): Acinetobacter Baumannii Atcc 19606 = Cip 70.34 = Jcm 6841

SUBMITTER: Hong Zeng

PROVIDER: PXD073438 | iProX | Fri Jan 23 00:00:00 GMT 2026

REPOSITORIES: iProX

ACCESS DATA

Similar Datasets

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.

Dataset Information

Nerol as an Anti-quorum sensing and Therapeutic Agent against Acinetobacter baumannii Pneumonia

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets