From: Extracellular vesicles in the pathogenesis and treatment of acute lung injury
EVs source | Molecules | Target cells | Effect | References |
---|---|---|---|---|
Human epithelial cell-EVs | miR-320a and miR-221 | Macrophages | Activated macrophage and facilitated the recruitment of immunomodulatory cells | [19] |
Vascular endothelial cell-EVs | CD31+ EVs | Alveolar macrophages | Anti-inflammatory and profibrotic effects | [24] |
Type II alveolar epithelial cell-EVs | CD74+ EVs | Alveolar macrophages | Pro-inflammatory and anti-fibrotic effects | [24] |
Alveolar macrophages-EVs | SOCS1 and SOCS3 | Alveolar epithelial cells | Suppressed allergic inflammation | |
Serum-exosomes | miR-1298-5p | BEAS-2B cells | Evoked inflammation, inhibited cell proliferation, and induced cell permeability | [74] |
T lymphocyte-derived EVs | Unknown | Airway epithelial cells | Reduced cell viability, promoted inflammatory cytokine production, and decreased anti-inflammatory cytokine levels | [77] |
Plasma-exosomes | S100A9 protein | HPMECs | Inhibited ZO-1 and occludin, and activated p38 MAPK signaling pathway/disruption of the tight junctions and endothelial barrier | [81] |
Circulating blood-exosomes | miR-1-3p | HUVECs | Inhibited cell proliferation, promoted apoptosis and cytoskeleton contraction, increased monolayer endothelial cell permeability and membrane injury | [82] |
Plasma-exosomes | miR-210-3p | THP-1 macrophage; BEAS-2B cells; HLMVECs | Enhanced THP-1 macrophage inflammation, BEAS-2B cell apoptosis, and HLMVEC permeability by regulating autophagy and inflammation activation | [84] |
Plasma-EVs | Surfactant protein C and GSDMD-p30 | Pulmonary vascular endothelial cells | Induced inflammatory injury and cell death | [85] |
MPMVEC-exosomes | Syndecan-1 protein | Lung tissues | Attenuated ALI and inhibited inflammation | [86] |
Peripheral serum-exosomes | miR-155 | Alveolar macrophages | Reduced SHIP1 and SOCS1, promoted macrophage proliferation and inflammation | [90] |
Activated neutrophils-derived EVs | miR-30d-5p | Alveolar macrophages | Induced polarization and apoptosis of M1 macrophages | [91] |
Alveolar epithelial cells-exosomes | miR-92a-3p | Alveolar macrophages | Induced pulmonary inflammation | [92] |
Alveolar epithelial cells-exosomes | miRNA | Alveolar macrophages | Activated inflammasomes and promoted lung inflammation | [93] |
Lung epithelial cell-EVs | Caspase-3 | Alveolar macrophages | Activated macrophages via the ROCK1 pathway | [94] |
Dust bacteria | Unknown | Airway epithelial cells | Increased the inflammatory cytokines and neutrophil infiltration | [99] |
Platelet | Unknown | Neutrophils | Mediated NETs formation | [100] |
Neutrophils | Unknown | Platelet | Promoted platelet activation | [101] |
Platelet | IL-1β and caspase-1 | Neutrophils | Attracted platelet-neutrophile aggregates | [102] |
Neutrophils | Neutrophil elastase and α−1 antitrypsin-resistance | Lung tissues | Destroyed lung extracellular matrix and alveolar structure | [103] |