This review highlights how extracellular vesicles mediate host defense, while pathogens exploit these mechanisms, suggesting therapeutic avenues.
Extracellular vesicles (EVs) released by host cells are emerging as central effectors of antibacterial immunity. Through distinct biogenetic pathways, they carry selectively sorted proteins, lipids, nucleic acids, and metabolites whose composition is dynamically reshaped by the physiological state of the producing cell. Infection-derived EVs propagate inflammatory and antimicrobial signals to bystander cells, intercept secreted bacterial toxins as molecular decoys, and prime adaptive responses through antigen presentation. Conversely, bacterial pathogens have evolved counterstrategies that suppress EV release, divert cargo loading, or co-opt EVs as carriers of virulence factors, thereby converting a host defence program into a pathogenic asset. The net outcome of EV-mediated communication is highly context-dependent, varying with pathogen species, host cell type, tissue environment, and infection stage. Here, we first review evidence that EVs serve as bona fide instruments of host defence, then describe how different bacterial pathogens subvert these same pathways, and discuss methodological limitations and translational opportunities for targeting infection-derived EVs.
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Fé et al. (2026) studied this question.
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