Bacterial extracellular vesicles: their role in antibiotic resistance and immune evasion
Antibiotic resistance is a rapidly escalating global healthcare crisis. Bacteria employ diverse strategies to evade both antibiotics and the host immune system. One of these tools is the use of bacterial extracellular vesi cles that mediate bacterial survival under antibiotic and immune stress. This review analyzes the impact of bacterial extracellular vesicles on antibiotic resistance and immune evasion. Bacterial extracellular vesicles of gram-positive and gram-negative bacteria have a number of structural differences, as well as different mechanisms for implementing their functions. Bacterial extracellular vesicles contribute to antibiotic resistance by acting as antibiotic targets, carrying resistance genes (horizontal gene transfer), and removing/degrading antibacterial agents. By implementing the strategy of evading immune surveillance, bacterial extracellular vesicles can participate in the formation of biofilms, provoke pro- and anti-inflammatory reactions, influence the secretion of cytokines by immune cells, creating more favorable conditions for colonization and development. Therefore, bacterial extracellular vesicles significantly contribute to bacterial survival under antibiotic and immune stress. However, the molecular mechanisms underlying bacterial extracellular vesi cles biogenesis and host responses to bacterial extracellular vesicles remain poorly understood, highlighting the need for further research to combat antibiotic resistance and bacterial infections.
Authors
- А. С. Головкин (ORCID: https://orcid.org/0000-0002-7577-628X)
- Anna Moiseeva (ORCID: https://orcid.org/0000-0001-7995-8235)
- K. N. Plekhanov
Institutions
- Federal Almazov North-West Medical Research Centre (RU)
Publication Details
- Journal
- Translational Medicine
- Published
- 2025-05-07
- DOI
- https://doi.org/10.18705/2311-4495-2025-12-1-94-107
- Primary Topic
- Bacterial Infections and Vaccines
- Type
- article
- Field-Weighted Citation Impact
- 0.00