ArticleCommunications biology2024
Experimental evolution under different nutritional conditions changes the genomic architecture and virulence of Acinetobacter baumannii.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Multi-omics uncovers the critical role of ceramide-mediatedJournal of pharmaceutical analysis · 2026Article
- Genomic and phenotypic analysis of multidrug-resistant Acinetobacter baumannii focusing on efflux pump activity and biofilm-associated genes.Molecular biology reports · 2026Article
- Resistance associated genomic variations for moderate level tigecycline resistance evolution in Acinetobacter baumannii.World journal of microbiology & biotechnology · 2026Article
- Periplasmic crowding and peptidoglycan hydrolase activity as drivers of outer membrane vesiculation in Acinetobacter baumannii.Communications biology · 2026Article
- Historical contingency limits adaptive diversification in a spatially structured environment.Evolution letters · 2026Article
- Sphingolipid-mediated vesiculation in multidrug-resistantApplied and environmental microbiology · 2025Article
- Comparative genome analysis of enterohemorrhagic Escherichia coli ATCC 43894 and its pO157-cured strain 277.Journal of microbiology (Seoul, Korea) · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
This study uncovers the molecular processes governing the adaptive evolution of multidrug-resistant (MDR) pathogens without antibiotic pressure. Genomic analysis of MDR Acinetobacter baumannii cells cultured for 8000 generations under starvation conditions (EAB1) or nutrient-rich conditions (EAB2) revealed significant genomic changes, primarily by insertion sequence (IS)-mediated insertions and deletions. Only two Acinetobacter-specific prophage-related deletions and translocations were observed in the EAB1 strain. Both evolved strains exhibited higher virulence in mouse infection studies, each with different modes of action. The EAB1 strain displayed a heightened ability to cross the epithelial barrier of human lung tissue, evade the immune system, and spread to lung tissues, ultimately resulting in cellular mortality. In contrast, the EAB2 strain strongly attached to epithelial cells, leading to increased synthesis of proinflammatory cytokines and chemokines. The genomic alterations and increased virulence observed in evolved strains during short-term evolution underscore the need for caution when handling these pathogens, as these risks persist even without antibiotic exposure.
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