The unusual suspects: the role of extracellular vesicles in host/pathogens interactions
Abstract
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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BibTeX
@article{fe2026unusual,
title = {{The unusual suspects: the role of extracellular vesicles in host/pathogens interactions}},
author = {Manon Le Fé and Matteo Bonazzi},
journal = {Current Opinion in Microbiology},
year = {2026},
month = oct,
doi = {10.1016/j.mib.2026.102797},
url = {https://hal.science/hal-05787582v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - The unusual suspects: the role of extracellular vesicles in host/pathogens interactions
AU - Manon Le Fé
AU - Matteo Bonazzi
PY - 2026
DA - 2026/10/08
JO - Current Opinion in Microbiology
DO - 10.1016/j.mib.2026.102797
UR - https://hal.science/hal-05787582v1
AB - 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.
SN - 1369-5274
SN - 1369-5274
ER -