Innate Immune System and Preeclampsia

Pérez-Sepúlveda, Alejandra; Torres, María José; Khoury, Maroun; Illanes, Sebastián E.

doi:10.3389/fimmu.2014.00244

Cited by 114 publications

(104 citation statements)

References 93 publications

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“…There are also findings that excessive activation of the innate immune system promotes the etiopathology of PE (134). Immunohistochemical studies revealed that there is increased expression of the CD14 macrophage marker in the decidua basalis from preterm preeclamptic versus preterm control pregnancies (157).…”

Section: Mice (Having Nk Cells But Not T or B Lymphocytes) Into Balb/mentioning

confidence: 99%

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Spradley

Palei

Granger

2015

American Journal of Physiology-Regulatory, Integrative and Comp

115

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) is a pregnancy-specific disorder typically presenting as new-onset hypertension and proteinuria. While numerous epidemiological studies have demonstrated that obesity increases the risk of PE, the mechanisms have yet to be fully elucidated. Growing evidence from animal and human studies implicate placental ischemia in the etiology of this maternal syndrome. It is thought that placental ischemia is brought about by dysfunctional cytotrophoblast migration and invasion into the uterus and subsequent lack of spiral arteriole widening and placental perfusion. Placental ischemia/ hypoxia stimulates the release of soluble placental factors into the maternal circulation where they cause endothelial dysfunction, particularly in the kidney, to elicit the clinical manifestations of PE. The most recognized of these factors are the anti-angiogenic sFlt-1 and pro-inflammatory TNF-␣ and AT1-AA, which promote endothelial dysfunction by reducing levels of the provasodilator nitric oxide and stimulating production of the potent vasoconstrictor endothelin-1 and reactive oxygen species. We hypothesize that obesity-related metabolic factors increase the risk for developing PE by impacting various stages in the pathogenesis of PE, namely, 1) cytotrophoblast migration and placental ischemia; 2) release of soluble placental factors into the maternal circulation; and 3) maternal endothelial and vascular dysfunction. This review will summarize the current experimental evidence supporting the concept that obesity and metabolic factors like lipids, insulin, glucose, and leptin affect placental function and increase the risk for developing hypertension in pregnancy by reducing placental perfusion; enhancing placental release of soluble factors; and by increasing the sensitivity of the maternal vasculature to placental ischemia-induced soluble factors. body mass index; inflammation; placental ischemia; pregnancy; RUPP; sFlt-1 PE IS A PREGNANCY-SPECIFIC DISORDER typically identified by new-onset hypertension in the second half of pregnancy. Although often accompanied by new-onset proteinuria, PE can be associated with many other signs and symptoms including headaches, visual disturbances, epigastric pain, and the development of edema (4,192). Globally, this disease affects over 8 million pregnancies per year and is estimated to account for 40 -60% of maternal deaths in developing countries (125). In the United States, there was a 25% increase in the rate of PE between the years 1987-2004 (189). This significant increase highlights the importance of understanding how risk factors like obesity play a role in the pathogenesis of this maternal syndrome. Obesity is defined as a body mass index (BMI) of greater than or equal to 30 kg/m 2 . Greater than one-half of pregnant women are overweight or obese (48), and more than two-thirds of reproductive-aged women in the United States are overweight or obese (49). Although mounting epidemiological evidence supports obesity as a major risk factor for PE, the mechanisms linking these two morbidities are...

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Section: Mice (Having Nk Cells But Not T or B Lymphocytes) Into Balb/mentioning

confidence: 99%

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Spradley

Palei

Granger

2015

American Journal of Physiology-Regulatory, Integrative and Comp

115

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“…9 During normal pregnancy, there is a shift toward T h 2 immunity that results in the synthesis of IL4, IL5, IL6, and IL10, whereas in PE there is a distinct shift toward T h 1 immunity, resulting in the production of IL2, TNFα, and IFNγ. 54 It is this shift toward T h 1-associated immunity in PE that results in the exaggerated MSIR. Therefore, T h 1-and T h 2-associated cytokines have gained interest as potential PE biomarkers.…”

Section: Cytokinesmentioning

confidence: 99%

Placenta-derived exosomes: potential biomarkers of preeclampsia

Pillay¹,

Moodley²,

Moodley³

et al. 2017

IJN

111

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Preeclampsia remains a leading cause of maternal and fetal mortality, due to ineffective treatment and diagnostic strategies, compounded by the lack of clarity on the etiology of the disorder. Although several clinical and biological markers of preeclampsia have been evaluated, they have proven to be ineffective in providing a definitive diagnosis during the various stages of the disorder. Exosomes have emerged as ideal biomarkers of pathological states, such as cancer, and have more recently gained interest in pregnancy-related complications, due to their role in cellular communication in normal and complicated pregnancies. This occurs as a result of the specific placenta-derived exosomal molecular cargo, which may be involved in normal pregnancy-associated immunological events, such as the maintenance of maternal–fetal tolerance. This review provides perspectives on placenta-derived exosomes as possible biomarkers for the diagnosis/prognosis of preeclampsia. Using keywords, online databases were searched to identify relevant publications to review the potential use of placenta-derived exosomes as biomarkers of preeclampsia.

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“…Although there have been great advances in medicine, the frequency of this disease has not been successfully modified significantly (3). Currently, the etiology of this disease remains unknown, therefore, in order to explain its origin various theories have been raised, and within each of them the genetic origin, immune factor, endothelial dysfunction, increased oxidative stress, micronutrients deficiency, among others, can be mentioned (3)(4)(5)(6)(7)(8). During pregnancy, there is a normal increase in the production of reactive oxygen species (ROS); likewise, the antioxidant capacity is increased.…”

Section: Introductionmentioning

confidence: 99%

Iodine levels are associated with oxidative stress and antioxidant status in pregnant women with hypertensive disease

et al. 2017

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Background: Previously has been reported the antioxidant function of iodine, and iodine deficiency as a risk factor of preeclampsia.Aim: We analyze the association between iodine deficiency, oxidative stress and antioxidant status with hypertensive disease of pregnancy (HPD).Method: 57 pregnant women were recruited in the last trimester of pregnancy, 20 diagnosed with hypertensive disease of pregnancy and 37 normotensive pregnant women. Urinary iodine concentration (UIC), TSH, free T4 (fT4), total antioxidant status (FRP), Superoxide dismutase (SOD), Catalase (CAT), and oxidative stress (TBARS) were evaluated by colorimetric methods.Results: UIC median for all pregnant women was of 151.9 µg / L. The UIC median for pregnant women with HPD was between 50-149 µg/L compared to 150-249 µg/L in normotensive women. No significant changes were found in levels of TSH and fT4 in normotensive pregnant compared with HPD women. Pregnant women with HPD had significant high levels of TBARS, and significant low levels of FRP, SOD, CAT and UIC compared to normotensive pregnant. In addition, pregnant women with optimal levels of UIC had a higher SOD activity (R = 0.354, P = 0.011), while iodine deficiency was associated with HPD (R = -0,281, p = 0.039). Similarly, pregnant with HPD had a significant negative association with SOD activity (R = -0,702, p = 0.005), CAT (R = -0,409, p = 0.002), and FRP (R = -0,624, p = 0.003), and a positive association with TBARS (R = 0.744, p = 0.001).Conclusion: iodine contributes to REDOX balance during pregnancy; its deficiency is associated with HPD. This study shows the importance of iodine during pregnancy.

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Innate Immune System and Preeclampsia

Cited by 114 publications

References 93 publications

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Placenta-derived exosomes: potential biomarkers of preeclampsia

Iodine levels are associated with oxidative stress and antioxidant status in pregnant women with hypertensive disease

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