Year: 2025
Type: article
Abstract: Acinetobacter baumannii relies on biofilms for antibiotic resistance, but the role of planktonic aggregates in drug tolerance is uncharacterized. We studied 103 clinical isolates to explore how the RND efflux pump gene adeG regulates aggregation. Non-MDR strains (with RND deletions) formed aggregates more frequently (13.79%, 4/29) than MDR strains (1.35%, 1/74), driven by residual RND efflux activity (not just deletions). adeG deletion induced 1–2 mm aggregates in a strain with combined adeR/ΔadeABC defects (via upregulated adhesion genes/hydrophobicity) but not in one with only ΔadeC. Aggregates boosted antibiotic tolerance (2–4-fold higher survival vs. disaggregated/parental strains) via metabolic dormancy (5-fold lower ATP), maintained growth in human serum, and promoted persistent bacteremia in immunosuppressed mice. Proteinase K disrupted aggregates, confirming protein matrices’ role. These findings identify planktonic aggregates as pivotal adaptive and virulence-related targets for combating refractory non-MDR A. baumannii infections while also revealing an association between adeG-related genetic contexts and aggregate formation in the bacterium.
Source: Microorganisms
Authors: Jiali Liu, Yinyue Li, Jie Liu, Zhiyong Tao, Feng Lu, Fang Tian, Jin-Hee Han, Xinlong He
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $3,258
Funder: Yangzhou University
OpenAlex ID: W4417499219
