The role of interleukins in preeclampsia: A comprehensive review

Abstract

Preeclampsia is a multi‐system hypertensive disorder of pregnancy, with significant rates of maternal and neonatal morbidity. It represents a major cause of preterm birth, as definitive treatment demands fetal delivery. Although its pathophysiology is complicated, placental hypoxia and endothelial dysfunction constitute established pathogenetic steps of the disease. Inflammation is considered to be a crucial mediator of preeclampsia process, as an imbalance between TH1, TH2, and TH17 immune responses is observed. The present review accumulates current knowledge about the contribution of interleukins in preeclampsia, summarizing the pathways through which each interleukin exerts its function in the disease. Also, the role of genetic polymorphisms is explored and the predictive efficacy of maternal serum interleukin levels is evaluated. Finally, recommendations about the safe interpretation of the outcomes, as well as guidance for future research, are provided.

The immunophenotype of decidual macrophages in acute atherosis

“…Moreover, acute atherosis has been linked to increased oxidative stress and lipid content in the decidua of preeclamptic women . Oxidative stress is also implicated in the pathophysiology of preeclampsia and fetal growth restriction . Hence, we proposed that macrophages are implicated in the mechanisms leading to oxidative stress, and therefore, obstetrical disease (ie, acute atherosis).…”

The prognostic role of serum uric acid levels in preeclampsia: A meta‐analysis

“…The pathophysiology of preeclampsia is complex and remains still under investigation. It is hypothesized that poor trophoblast invasion and deficient spiral artery remodeling lead to placental ischemia‐reperfusion injury 4 and the release of various angiogenic, 5 oxidative, 6 and inflammatory 7 mediators into maternal circulation, promoting generalized endothelial dysfunction, increased vascular reactivity, and activation of the coagulation cascade 8 . Risk stratification is essential in order to identify the subpopulation of pregnant women that would benefit from preventive measures early in the course of gestation, especially the administration of aspirin 9 .…”

A rat model of placental inflammation explains the unexplained elevated maternal serum alpha‐fetoprotein associated with adverse pregnancy outcomes

“…Most APO can trace their origins to placenta, especially to placental inflammation/infection . Pre‐eclampsia and fetal growth restriction are rooted in defects of early placental development and later placental inflammation (the two‐stage model) . Stillbirth and fetal growth restriction are associated with placental inflammation due to infectious or noninfectious causes .…”

“…9 Preeclampsia and fetal growth restriction are rooted in defects of early placental development and later placental inflammation (the two-stage model). 9,10 Stillbirth and fetal growth restriction are associated with placental inflammation due to infectious or noninfectious causes. 9 A recent morphological study showed that inflammation/infection and malperfusion were the two most common pathological changes in the placentas of preterm birth.…”