Increased Endothelial Monocyte Chemoattractant Protein-1 and Interleukin-8 in Preeclampsia

Abstract

In Brief OBJECTIVE To test the hypothesis that preeclampsia is associated with increased endothelial cell chemokine production of monocyte chemoattractant protein-1 and interleukin-8 necessary for monocyte recruitment to the vascular endothelium. METHODS Plasma was collected from women with severe preeclampsia and normal pregnant women at term and measured for monocyte chemoattractant protein-1, interleukin-8, and lipid peroxide levels by enzyme-linked immunosorbent assays and malondialdehyde assays. Human umbilical vein endothelial cells were cultured with 5% plasma from normal or preeclamptic patients and the media assayed for monocyte chemoattractant protein-1 and interleukin-8 production. RESULTS In women with severe preeclampsia, plasma levels of monocyte chemoattractant protein-1, interleukin-8, and lipid peroxides were elevated (1.5-fold, 2.5-fold, and 4.5-fold higher, respectively) compared with normal pregnant women. Human umbilical vein endothelial cells cultured with plasma from preeclamptic women significantly increased the production of both monocyte chemoattractant protein-1 (2.3-fold) and interleukin-8 (1.5-fold) compared with plasma from normal pregnant women. Monocyte chemoattractant protein-1 and interleukin-8 production was decreased by the antioxidant vitamin E in human umbilical vein endothelial cells treated with preeclamptic plasma, suggesting that the production of these cytokines may be regulated by signaling mechanisms sensitive to oxidative stress. CONCLUSION These findings support the hypothesis that circulating factors in the plasma of women with preeclampsia activate endothelial cell monocyte chemoattractant protein-1 and interleukin-8 production, and although not directly examined in this study, may increase monocyte adherence to the vascular endothelium. Plasma from women with severe preeclampsia has increased monocyte chemoattractant protein-1 and interleukin-8 and stimulates the production of these chemokines in vascular endothelial cells.