Fig 1.
Types and biogenesis of bacterial, fungal, and parasitic EVs.
Gram-negative bacteria can produce EVs through 2 mechanisms: membrane blebbing and explosive cell lysis. OMVs and OIMVs originate from membrane blebbing, while EOMVs and EOIMVs originate from explosive cell lysis. Gram-positive bacteria can produce CMVs through bubbling cell death. Additionally, fungi and parasites can produce EVs through 2 pathways: cell endocytosis and membrane budding. Exosomes are derived from cell endocytosis and ectosomes originate from membrane budding. EVs, extracellular vesicles; OMVs, outer membrane vesicles; OIMVs, outer-inner membrane vesicles; EOMVs, explosive outer membrane vesicles; EOIMVs, explosive outer-inner membrane vesicles; CMVs, cytoplasmic membrane vesicles. The figure was designed using Biorender.
Fig 2.
Bacterial EVs contribute to antibiotic resistance through multiple mechanisms.
(A) EVs can act as decoys to bind to membrane-targeting antibiotics. (B) EVs can act as decoys to encapsulate antibiotics during formation. (C) EVs can degrade antibiotics through enzymes. (D) EVs can transfer resistance genes to recipient cells, mediating the spread of resistance. EVs, extracellular vesicles. The figure was designed using Biorender.
Fig 3.
Bacterial EVs contribute to antimicrobial therapy.
(1) Bacterial EVs may possess natural antibacterial activity to directly kill pathogens. (2) Bacterial EVs can be loaded with antibiotics, enhancing the targeting, affinity and stability of antibiotics. (3) Bacterial EVs can mimic the bacterial outer membrane and be used to assess the permeability of antibiotics. EVs, extracellular vesicles. The figure was designed using Biorender.