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Biomolecules 2015, 5(4), 3142-3176; doi:10.3390/biom5043142

Immune Mechanisms Linking Obesity and Preeclampsia

Department of Physiology and Biophysics, Cardiovascular-Renal Research Center, Women’s Health Research Center, The University of Mississippi Medical Center, Jackson, MS 39216, USA
Denotes co-first authors.
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Author to whom correspondence should be addressed.
Academic Editor: Ivana Vancurova
Received: 23 July 2015 / Revised: 7 October 2015 / Accepted: 20 October 2015 / Published: 12 November 2015
(This article belongs to the Special Issue Transcriptional Regulation of Pro-Inflammatory Genes)
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Abstract

Preeclampsia (PE) is characterized by hypertension occurring after the twentieth week of pregnancy. It is a significant contributor to maternal and perinatal morbidity and mortality in developing countries and its pervasiveness is increasing within developed countries including the USA. However, the mechanisms mediating the pathogenesis of this maternal disorder and its rising prevalence are far from clear. A major theory with strong experimental evidence is that placental ischemia, resulting from inappropriate remodeling and widening of the maternal spiral arteries, stimulates the release of soluble factors from the ischemic placenta causing maternal endothelial dysfunction and hypertension. Aberrant maternal immune responses and inflammation have been implicated in each of these stages in the cascade leading to PE. Regarding the increased prevalence of this disease, it is becoming increasingly evident from epidemiological data that obesity, which is a state of chronic inflammation in itself, increases the risk for PE. Although the specific mechanisms whereby obesity increases the rate of PE are unclear, there are strong candidates including activated macrophages and natural killer cells within the uterus and placenta and activation in the periphery of T helper cells producing cytokines including TNF-α, IL-6 and IL-17 and the anti-angiogenic factor sFlt-1 and B cells producing the agonistic autoantibodies to the angiotensin type 1 receptor (AT1-aa). This review will focus on the immune mechanisms that have been implicated in the pathogenesis of hypertension in PE with an emphasis on the potential importance of inflammatory factors in the increased risk of developing PE in obese pregnancies. View Full-Text
Keywords: Adipose; antibody; endothelin; hypertension; lymphocyte; pregnancy Adipose; antibody; endothelin; hypertension; lymphocyte; pregnancy
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MDPI and ACS Style

Spradley, F.T.; Palei, A.C.; Granger, J.P. Immune Mechanisms Linking Obesity and Preeclampsia. Biomolecules 2015, 5, 3142-3176.

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