Microbial extracellular vesicles (EVs) play a significant role in antimicrobial resistance. This review summarizes the roles and mechanisms of bacterial, fungal, and parasitic EVs in promoting antimicrobial resistance and discusses the potential applications of bacterial EVs in antimicrobial therapy. EVs are nanoscale vesicles that can transfer biomolecules like proteins, lipids, and nucleic acids, facilitating inter-microbial communication and microbial adaptation to environmental stress. Bacterial EVs contribute to antimicrobial resistance through multiple mechanisms. They can act as decoys to bind or encapsulate antibiotics, degrade antibiotics through enzymes, and transfer resistance genes to recipient cells. For example, OMVs from Escherichia coli can bind to polymyxin B to protect bacteria, while CMVs from Staphylococcus aureus can bind to daptomycin. Additionally, bacterial EVs can degrade antibiotics by transporting β-lactamases, which hydrolyze antibiotics. EVs can also transfer resistance genes, such as blaKPC-2 and blaNDM-1, between bacteria, promoting the spread of resistance. Fungal EVs contribute to antimicrobial resistance by participating in the biogenesis of the biofilm matrix and by repairing and remodeling the cell wall. For instance, fungal biofilm-derived EVs can increase biofilm thickness and metabolic activity, enhancing resistance to antifungal drugs. Additionally, fungal EVs can transfer cell wall-associated proteins, which help in cell wall repair and resistance to antifungal agents. Parasitic EVs also contribute to antimicrobial resistance by transferring drug resistance genes and proteins between parasites. For example, Plasmodium falciparum EVs can transfer resistance genes to other P. falciparum, leading to the spread of drug resistance. Similarly, Leishmania EVs can transfer resistance genes and reduce oxidative stress in recipient cells, promoting their growth and adaptability. Bacterial EVs have potential applications in antimicrobial therapy. They possess natural antimicrobial activity and can be used to deliver antibiotics, enhancing their targeting, affinity, and stability. Bacterial EVs can also mimic the bacterial outer membrane, aiding in the assessment of antibiotic permeability. These properties make bacterial EVs promising candidates for developing new antimicrobial strategies. However, challenges such as the difficulty of large-scale preparation and surface modification remain. Further research is needed to fully harness the potential of bacterial EVs in antimicrobial therapy.Microbial extracellular vesicles (EVs) play a significant role in antimicrobial resistance. This review summarizes the roles and mechanisms of bacterial, fungal, and parasitic EVs in promoting antimicrobial resistance and discusses the potential applications of bacterial EVs in antimicrobial therapy. EVs are nanoscale vesicles that can transfer biomolecules like proteins, lipids, and nucleic acids, facilitating inter-microbial communication and microbial adaptation to environmental stress. Bacterial EVs contribute to antimicrobial resistance through multiple mechanisms. They can act as decoys to bind or encapsulate antibiotics, degrade antibiotics through enzymes, and transfer resistance genes to recipient cells. For example, OMVs from Escherichia coli can bind to polymyxin B to protect bacteria, while CMVs from Staphylococcus aureus can bind to daptomycin. Additionally, bacterial EVs can degrade antibiotics by transporting β-lactamases, which hydrolyze antibiotics. EVs can also transfer resistance genes, such as blaKPC-2 and blaNDM-1, between bacteria, promoting the spread of resistance. Fungal EVs contribute to antimicrobial resistance by participating in the biogenesis of the biofilm matrix and by repairing and remodeling the cell wall. For instance, fungal biofilm-derived EVs can increase biofilm thickness and metabolic activity, enhancing resistance to antifungal drugs. Additionally, fungal EVs can transfer cell wall-associated proteins, which help in cell wall repair and resistance to antifungal agents. Parasitic EVs also contribute to antimicrobial resistance by transferring drug resistance genes and proteins between parasites. For example, Plasmodium falciparum EVs can transfer resistance genes to other P. falciparum, leading to the spread of drug resistance. Similarly, Leishmania EVs can transfer resistance genes and reduce oxidative stress in recipient cells, promoting their growth and adaptability. Bacterial EVs have potential applications in antimicrobial therapy. They possess natural antimicrobial activity and can be used to deliver antibiotics, enhancing their targeting, affinity, and stability. Bacterial EVs can also mimic the bacterial outer membrane, aiding in the assessment of antibiotic permeability. These properties make bacterial EVs promising candidates for developing new antimicrobial strategies. However, challenges such as the difficulty of large-scale preparation and surface modification remain. Further research is needed to fully harness the potential of bacterial EVs in antimicrobial therapy.