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Published on: July 7, 2020
Circulating Outer Membrane Vesicles from Gut-Colonized Carbapenem-Resistant Enterobacterales Degrade Antibiotics and
Peifen Li1, Yingying Lin1, Xihuan Sun1
1Clinical Microbiology Laboratory, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian, People's Republic of China.
Purpose:
Gut colonization of carbapenem-resistant Enterobacterales (CRE) poses a significant risk for systemic infections, but the mechanisms driving resistance dissemination are poorly understood. This study aimed to investigate whether outer membrane vesicles (OMVs) secreted by gut-colonized CRE can enter the human circulatory system and mediate extracellular antibiotic resistance through functional carbapenemases and resistance genes.
Patients And Methods:
We conducted comparative proteomic analyses of OMVs isolated from parental CRE strains and patient plasma samples. Antibiotic degradation assays were performed to evaluate OMV-mediated hydrolysis of imipenem and meropenem. In vitro experiments assessed the protective effects of OMVs on carbapenem-susceptible Escherichia coli and Pseudomonas aeruginosa. Additionally, a Galleria mellonella infection model was used to examine OMV-mediated bacterial survival under carbapenem pressure.
Results:
Plasma-derived OMVs exhibited proteomic profiles similar to bacterial OMVs, including carbapenemase components, and demonstrated comparable antibiotic-degrading activity. These OMVs hydrolyzed 60-75% of imipenem and meropenem within 24 hours, protecting susceptible bacteria from growth inhibition in vitro. Although no horizontal gene transfer was observed, OMVs enhanced Klebsiella pneumoniae survival under carbapenem pressure in the G. mellonella model, increasing larval survival rates by 25%.
Conclusion:
Our findings reveal a novel OMV-mediated extracellular resistance mechanism that operates independently of genetic transfer, promoting bacterial persistence in the bloodstream. This study provides key insights into the role of OMVs in clinical treatment failure and identifies potential therapeutic targets to combat antibiotic resistance dissemination.
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