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Circulating Cluster of Differentiation CD3 Cells Derived Extracellular Vesicles Are Increased in Chronic Pulmonary Vascular Diseases
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A2075 - Circulating Cluster of Differentiation CD3 Cells Derived Extracellular Vesicles Are Increased in Chronic Pulmonary Vascular Diseases
Author Block: U. Deo; Med. clinic II, UKGM, ECCPS, Giessen, Germany.
Rationale: Extracellular vesicles (EVs) are cell membrane-derived structures released during different cellular processes, such as activation or apoptosis. Circulating endothelial cell-derived and procoagulant microparticles (MPs), which are a type of EVs, are found to be increased in patients with pulmonary hypertension (PH). Literature indicated that inflammatory cells-derived MPs may play a role in various inflammatory health disorders. Following the fact that PH is described as a disease with altered inflammation, we hypothesized that inflammatory cells-derived EVs are involved in the pathology of PH.
Methods: The central blood from patients with different forms of PH (idiopathic/heritable pulmonary arterial hypertension (PAH), associated PAH, PH due to chronic obstructive pulmonary disease, PH associated with pulmonary fibrosis, PH due to left heart disease and chronic thromboembolic PH) (n=5-14) and non-PH controls (n=6-8) was collected during right-heart catheterization, and the platelet-free plasma (PFP) was prepared. PFP was used for flow cytometry analysis of different circulating inflammatory cells-derived EVs (CD3 (T-cells), CD14 (macrophages/monocytes) and CD68 (macrophages)).
Results: The flow cytometry characterization revealed that circulating CD3 cells-derived EVs (events/µl) were enhanced in all of the above mentioned clinical groups of PH, in comparison to the non-PH controls. Conversely, there were no prominent alterations in the circulating levels of CD14 and CD68 cells-derived EVs in various PH forms, compared to the non-PH controls. Surprisingly, there was just a moderate and non-significant positive correlation between circulating levels of CD3 cells-derived EVs and the relevant clinical parameters of PH, such as mean pulmonary arterial pressure (mmHg) and pulmonary vascular resistance (dyn*s*cm-5).
Conclusions: Our study identified an augmented levels of circulating T cells-derived EVs in several different forms of PH. Therefore, this EVs may represent a novel player in the pathogenesis of the severe pulmonary vascular diseases. The future studies should focus to reveal in details the precise role of T cells-derived EVs, which may represent active contributors to the disease development and/or progression, knowing the fact that EVs may carry different mediators, such as micro RNAs.
Author Block: U. Deo; Med. clinic II, UKGM, ECCPS, Giessen, Germany.
Rationale: Extracellular vesicles (EVs) are cell membrane-derived structures released during different cellular processes, such as activation or apoptosis. Circulating endothelial cell-derived and procoagulant microparticles (MPs), which are a type of EVs, are found to be increased in patients with pulmonary hypertension (PH). Literature indicated that inflammatory cells-derived MPs may play a role in various inflammatory health disorders. Following the fact that PH is described as a disease with altered inflammation, we hypothesized that inflammatory cells-derived EVs are involved in the pathology of PH.
Methods: The central blood from patients with different forms of PH (idiopathic/heritable pulmonary arterial hypertension (PAH), associated PAH, PH due to chronic obstructive pulmonary disease, PH associated with pulmonary fibrosis, PH due to left heart disease and chronic thromboembolic PH) (n=5-14) and non-PH controls (n=6-8) was collected during right-heart catheterization, and the platelet-free plasma (PFP) was prepared. PFP was used for flow cytometry analysis of different circulating inflammatory cells-derived EVs (CD3 (T-cells), CD14 (macrophages/monocytes) and CD68 (macrophages)).
Results: The flow cytometry characterization revealed that circulating CD3 cells-derived EVs (events/µl) were enhanced in all of the above mentioned clinical groups of PH, in comparison to the non-PH controls. Conversely, there were no prominent alterations in the circulating levels of CD14 and CD68 cells-derived EVs in various PH forms, compared to the non-PH controls. Surprisingly, there was just a moderate and non-significant positive correlation between circulating levels of CD3 cells-derived EVs and the relevant clinical parameters of PH, such as mean pulmonary arterial pressure (mmHg) and pulmonary vascular resistance (dyn*s*cm-5).
Conclusions: Our study identified an augmented levels of circulating T cells-derived EVs in several different forms of PH. Therefore, this EVs may represent a novel player in the pathogenesis of the severe pulmonary vascular diseases. The future studies should focus to reveal in details the precise role of T cells-derived EVs, which may represent active contributors to the disease development and/or progression, knowing the fact that EVs may carry different mediators, such as micro RNAs.
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