Indirect effect of PM on endothelial cells via inducing the release of respiratory inflammatory cytokines.

A large number of epidemiological studies have shown that increased cardiovascular morbidity and mortality are associated with exposure to high concentrations of PM. One of the ways that PM affects the cardiovascular system is through systemic inflammation. Inflammatory cytokines such as TNF-α, IL-1β, IL-6, and IL-8 stimulate endothelial cells, which leads to endothelial dysfunction. Compared with PM, PM is smaller in size, has a larger surface area and absorbs more toxic substances such as heavy metals, organic compounds, and black carbon. However, the effect of PM on human health is less studied. Here, we used BEAS-2B cells and differentiated THP-1 cells to simulate epithelial cells and macrophages in the lung, respectively. The indirect effect of PM on endothelial cells was studied with a coculture model consisting of two cell lines (BEAS-2B cells and macrophages) in the top compartment and one cell line, human umbilical vein endothelial cells (EA.hy926), in the bottom compartment of a transwell plate. The results showed that PM could promote the release of inflammatory cytokines, including TNF-α and IL-6, from BEAS-2B cells and macrophages. In addition, PM upregulated ICAM-1 expression in EA.hy926 cells through TNF-α/NF-κB signaling pathways, promoting the adhesion of endothelial cells and monocytes, a key event in the initiation of atherosclerosis.