Abstract
Exposure to particulate matter (PM) is becoming a major global health issue. The amount and time of exposure to PM are known to be closely associated with cardiovascular diseases. However, the mechanism through which PM affects the vascular system is still not clear. Endothelial cells line the interior surface of blood vessels and actively interact with plasma proteins, including the complement system. Unregulated complement activation caused by invaders, such as pollutants, may promote endothelial inflammation. In the present study, we sought to investigate whether urban PM (UPM) acts on the endothelial environment via the complement system. UPM-treated human endothelial cells with normal human serum showed the deposition of membrane attack complexes (MACs) on the cell surface via the alternative pathway of the complement system. Despite the formation of MACs, cell death was not observed, and cell proliferation was increased in UPM-mediated complement activation. Furthermore, complement activation on endothelial cells stimulated the production of inflammation-related proteins. Our results revealed that UPM could activate the complement system in human endothelial cells and that complement activation regulated inflammatory reaction in microenvironment. These findings provide clues with regard to the role of the complement system in pathophysiologic events of vascular disease elicited by air pollution.
Highlights
Particulate matter (PM) is a mixture of microscopic particles with complex compositions suspended in the atmosphere; it mostly arises from the combustion of fossil fuels or road dust
A significant decrease in cell viability and an increase in cell death were observed at 48 h after treatment with 50 to 200 μg/mL urban PM (UPM) compared to the untreated control (Figure 1a,b)
To investigate whether exposure to UPM can result in complement activation, we examined the deposition of membrane attack complexes (MACs) or C5b-9 on untreated and UPM-treated human umbilical vein endothelial cells (HUVECs) at 48 h following incubation of the cells with normal human serum (NS) for 1 h
Summary
Particulate matter (PM) is a mixture of microscopic particles with complex compositions suspended in the atmosphere; it mostly arises from the combustion of fossil fuels or road dust. The smaller the size of the particles, the more likely they are to escape the respiratory defense mechanism and invade deep into the respiratory tract, which can directly affect the cells lining the alveolar wall [4]. PM is known to be associated with respiratory diseases [5] and with cardiovascular and immunological disorders [6,7]. PM with a diameter of less than 2.5 μm can enter systemic circulation through gaps formed between alveolar epithelial cells [8]. PM in air pollution disrupts the endothelium and induces an inflammatory reaction, which is correlated to cardiovascular diseases [6,9,10]. The pathophysiologic mechanisms underlying the association between PM and cardiovascular disease are not fully understood
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