Maternal Serum Levels of TNF-Alpha and IL-6 Long after Delivery in Preeclamptic and Normotensive Pregnant Women

Abstract

Aim. To evaluate maternal TNF-alpha and IL-6 plasma levels in normotensive pregnant women, women with preeclampsia, and to examine the temporal changes in their levels from theantepartum to the postpartum period correlated with the regression of preeclampsia. Method. A prospective study was performed in the 2nd Department of Obstetrics and Gynecology, University of Athens. Blood samples were obtained: (1) antepartum at the time of clinical diagnosis of the syndrome, 2. 12-14 weeks postpartum. Results. No statistically significant differences were found in IL-6 levels, whereas a difference was found in TNF-alpha levels between preeclamptic and controls in antepartum period (0.80 pg/ml versus 0.60 pg/ml, P : .04). Long after delivery, TNF-alpha levels were significantly higher in preeclamptic compared to normotensive controls (0.86 pg/ml versus 0.60 pg/ml, P : .004). No difference was observed in TNF-alpha before and after delivery in both groups. No difference was noticed in IL-6 levels in women of normotensive group long after delivery compared to that before delivery. Long after delivery IL-6 levels were statistically significant higher in preeclamptic women compared to normal controls (3.53 ± 0.52 pg/ml versus 1.69 ± 0.48 pg/ml, P : .02). Conclusion. Preeclamptic women remain under a status of increased inflammatory stress up to 12-14 weeks postpartum despite the fact that all the other signs of preeclampsia are resolved.

Assessment of angiogenesis modulators in pregnant women with pre-eclampsia: a case–control study

“…It is known that this cytokine induces trophoblastic apoptosis, through the overproduction of free radicals by macrophages and monocytes [32]. Thus, it is expected that the serum levels of this cytokine would be elevated in PE [32,33].…”

“…It is known that this cytokine induces trophoblastic apoptosis, through the overproduction of free radicals by macrophages and monocytes [32]. Thus, it is expected that the serum levels of this cytokine would be elevated in PE [32,33]. Roudsari et al [34], assessing TNF-a, did not find a statistically significant difference between pregnant women with PE and their normotensive peers, observing low and stable serum levels during pregnancy; their results are in agreement with those of the present study.…”

Maternal plasma concentrations of sST2 and angiogenic/anti-angiogenic factors in preeclampsia

“…First, a higher plasma sST2 concentration may be a consequence of an intravascular inflammatory response which is exacerbated in preeclampsia when compared to an uncomplicated pregnancy [23,25,[168][169][170]. Indeed, it has been demonstrated that pro-inflammatory cytokines are increased in the plasma or serum of women with early-onset preeclampsia [35,41,42] and severe preeclampsia [36,40,41] when compared to women with uncomplicated pregnancies. Moreover, IL-1b or TNF-a (pro-inflammatory cytokines which are increased in preeclampsia) are able to stimulate vascular endothelial cells to secrete sST2 into supernatant [146,147].…”

“…A defect of deep placentation [9][10][11][12][13] is proposed to generate utero-placental ischemia [14][15][16], placental endoplasmic reticulum and oxidative stress [17][18][19][20][21][22], and subsequently systemic intravascular inflammation [23][24][25] and endothelial dysfunction [17,[26][27][28][29][30][31][32][33][34]. The circulating concentrations of pro-inflammatory cytokines, such as interleukin (IL)-1-b and tumor necrosis factor (TNF)-a [35][36][37][38][39], as well as other inflammatory mediators (such as IL-6) [36,[40][41][42] are typically elevated in patients with preeclampsia, although this is not a universal feature [43,44]. The placenta is essential for the development of preeclampsia, while the fetus is not [45][46][47].…”

Association of Inflammatory Cytokines, Lipid Peroxidation End Products and Nitric Oxide with the Clinical Severity and Fetal Outcome in Preeclampsia in Indian Women

“…TNF-a inhibits decidual invasion by cytotrophoblasts, stimulates cell proliferation and hypoxia-mediated cell activation. It also induces structural and functional alterations in endothelial cells, endothelin-1 (ET-1) production and inhibition of acetylcholine induced vasodilatation [11,12].…”