In Vitro Study of Ambient Air Pollutants on Endothelial Cells
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Date
2013-05
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The Ohio State University
Abstract
Ambient fine particulate matter (PM2.5, diameter less than 2.5 μm) is a major component of air pollutants. Because of the small sizes of particulate categorized as PM2.5, it can easily be inhaled deeply into the lungs and deposit in the alveoli. These small particles may cross the air-liquid interface, enter the blood stream, and spread to the rest of the body. Studies over the past few decades have linked PM2.5 to different health consequences including cardiovascular diseases by causing local or systemic damage. Moreover, it has been well recognized that toxicity of PM2.5 depends, in part, on the specific chemical composition of the particles, such as the metals Ni, Mn, Al, Cu, which are often implicated as causative agents of disease. Currently, it is known that PM2.5 can exacerbate inflammation of endothelial tissues, leading to health defects including cardiovascular disease, insulin resistance, and type II diabetes.
Among the PM2.5 and Ni exposed tissues, we are specifically interested in the endothelium. Local macrophages could be activated by this air contaminant combination. In turn, the activated macrophages will recruit more circulating macrophages to this specific region and induce local inflammation. This is especially important because local inflammation is a key player in suppressing eNOS which supports vasal activity.
Hence, we tested the hypotheses that the exposure to PM2.5 in combination with a transition metal such as Ni would result in inflammatory responses as well as a reduction of vasodilatation through the endothelial nitric oxidase synthase (eNOS) related pathways. The chemotaxis of murine macrophage-like cell line RAW 264.7 was activated by PM2.5 and further induced with the addition of Ni particles. The activated M1 like macrophages in turn induced more macrophage accumulation. In terms of endothelial function, the suppressed eNOS expression by activated macrophages and local inflammation implies the loss of vassal activity.
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PM2.5 Ni Inflammation eNOS