Extracellular vesicles in the pathogenesis and treatment of acute lung injury

Hu, Qian; Zhang, Shu; Yang, Yue; Yao, Jia-Qi; Tang, Wen-Fu; Lyon, Christopher J.; Hu, Tony Ye; Wan, Mei-Hua

doi:10.1186/s40779-022-00417-9

Military Medical Research

Table 1 EVs participate in ALI/ARDS by regulating alveolar cells

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	[25, 78]
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]

ALI acute lung injury, ARDS acute respiratory distress syndrome, BEAS-2B human bronchial epithelial cells, EVs extracellular vesicles, HLMVECs human lung microvascular endothelial cells, HPMECs human pulmonary microvascular endothelial cells, HUVECs human umbilical vein endothelial cells, IL-1β interleukin-1β, MPMVECs mouse pulmonary microvascular endothelial cells, NETs neutrophil extracellular traps, SHIP1 SH2 domain-containing inositol phosphatese1, SOCS1 suppressor of cytokine signaling 1, SOCS3 suppressor of cytokine signaling 3, S100A9 S100 calcium binding protein A9, ZO-1 zonula occludens-1

Back to article page

ISSN: 2054-9369

Contact us

Submission enquiries: Access here and click Contact Us
General enquiries: info@biomedcentral.com