Association between higher expression of interleukin-8 (IL-8) and haplotype −353A/−251A/+678T of IL-8 gene with preeclampsia

Mao, Dongwei; Cai, Yan; Tan, Weihong; Hao, Yanlan; Liu, Lin; Liu, Wei

doi:10.1097/md.0000000000005537

Cited by 28 publications

(27 citation statements)

References 24 publications

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“…Our results about the placental gene expression of IL-6 also concur with Marusic et al [10] and Benyo et al [11]. With respect to IL-8, Sun et al [13] reported higher levels of gene expression of this cytokine in PE in comparison to the term control group by real-time RT-PCR; however, their sampling method was susceptible to bias because they analyzed only 1 point of the maternal side of the placenta. We did not observe a difference in the IL-8 gene expression, but there was a difference in the IL-8/ IL-RA placental ratio, which was higher in PE than NP.…”

Section: Discussionsupporting

confidence: 78%

Placental Proinflammatory State and Maternal Endothelial Dysfunction in Preeclampsia

Valencia

Zárate

Saucedo

et al. 2018

Gynecol Obstet Invest

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Objective: To evaluate the placental and decidual gene expression and maternal and umbilical serum concentrations of tumor necrosis factor alpha, interleukin 6 (IL-6), IL-8, IL-10, IL-1 receptor antagonist (IL-1RA), intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 (VCAM-1), along with the proinflammatory/anti-inflammatory cytokine ratios in women with preeclampsia (PE) vs. women with normal pregnancy (NP), and to analyze PE classified as early- (EO) and late-onset (LO). Methods: This cross-sectional study was performed with 50 women with PE (EO n = 30, LO n = 20) and 50 women with NP. Tissue gene expression levels were measured by real-time RT-PCR. Cytokines and adhesion molecules serum concentrations were measured by immunoassays. Results: In PE, placental expression of IL-10 and IL-1RA was lower, while placental IL-8/IL-1RA ratio and maternal concentrations of VCAM-1 were higher vs. NP. In EO, placental expression of IL-10 was lower, while placental IL-8/IL-10 and IL-8/IL-1RA ratios were higher than LO and NP. Maternal concentrations of IL-6 were higher in LO than EO and NP. Throughout PE, maternal VCAM-1 concentrations were higher vs. NP. No significant differences were observed in the decidual expression and umbilical concentrations of the markers between the groups. Conclusion: PE associates with a proinflammatory placental state; however, EO associates with a proinflammatory placental state, while LO associates with systemic maternal inflammation. Both subtypes associated with maternal endothelial dysfunction.

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Section: Discussionsupporting

confidence: 78%

Placental Proinflammatory State and Maternal Endothelial Dysfunction in Preeclampsia

Valencia

Zárate

Saucedo

et al. 2018

Gynecol Obstet Invest

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“…Farina et al, notably under a prospective study design, found significantly increased IL‐8 levels in chorionic villous samples of PE women. Sun et al used immunochemistry and quantitative real‐time polymerase chain reaction (qPCR) techniques and demonstrated that placentas derived from PE pregnancies exhibit significantly increased mRNA and protein expression of IL‐8. In the same study, the incidence of IL‐8‐251A allele was found to be higher in women with PE, while the haplotype −353A/−251A/+678T (AAT) was identified as risk factor for the development of the disease.…”

Section: Resultsmentioning

confidence: 99%

The role of interleukins in preeclampsia: A comprehensive review

Bellos

Karageorgiou

Kapnias

et al. 2018

American J Rep Immunol

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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.

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“…Moreover, human placental tissue produces IL-8 during pregnancy. Previous studies showed a robust correlation between IL-8 levels and the severity of PE ( 5 , 15 ) . Neutrophil activation results in progressive damage to endothelial cells ( 16 ) .…”

Section: Introductionmentioning

confidence: 83%

“…In the pathogenesis of PE, activation of neutrophils, monocytes, and natural killer cells initiate inflammation, resulting in endothelial destruction in the pathogenesis of PE ( 4 ) . The damaged endothelium produces various chemokines, one of which is interleukin (IL)-8 ( 5 ) .…”

Section: Introductionmentioning

confidence: 99%

Endothelial cell leptin receptors, leptin and interleukin-8 in the pathogenesis of preeclampsia: An in-vitro study

Arlıer¹

2017

tjod

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Objective:Increased leptin hormone and leptin receptor may enhance the generation of proinflammatory cytokines by endothelial cells and lead to endothelial dysfunction. This study assessed the umbilical cord endothelial leptin receptor levels in preeclampsia and investigated the effect of leptin on endothelial interleukin-8 (IL-8) production.Materials and Methods:The association between IL-8 levels with leptin stimulation was investigated in leptin-treated human endothelial cells. Endothelial cell leptin receptor levels were evaluated using immunohistochemistry staining, and endothelial IL-8 protein expression by Western blot analysis. Data are presented as mean ± standard error of the mean (SEM). Statistical significance was analyzed using Student’s t-test or Mann-Whitney U test and one-way analysis of variance.Results:Leptin receptor immunoreactivity increased significantly in umbilical cord venous and arterial endothelial cells in normal pregnancy (n=12) compared with preeclampsia (n=7) endothelial cells. The corresponding preeclampsia versus control histologic scores (mean ± SEM) were 67.9±8.8 vs. 127.6±23.1, (p=0.011) for the leptin receptor and 55.4±8,0 vs. 93.7±17.1 (p=0.035), respectively, for the vein endothelial cells. Leptin treatment significantly increased IL-8 protein levels (control vs. 100 and 1000 ng/mL, p=0.003).Conclusion: The findings of increased umbilical cord endothelial leptin receptor levels in preeclampsia and increased endothelial IL-8 expression with exposure to higher leptin concentrations may indicate the contribution of leptin to endothelial dysfunction and increased neutrophil-endothelial interaction, which are significant pathophysiologic features of preeclampsia.

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Association between higher expression of interleukin-8 (IL-8) and haplotype −353A/−251A/+678T of IL-8 gene with preeclampsia

Cited by 28 publications

References 24 publications

Placental Proinflammatory State and Maternal Endothelial Dysfunction in Preeclampsia

Placental Proinflammatory State and Maternal Endothelial Dysfunction in Preeclampsia

The role of interleukins in preeclampsia: A comprehensive review

Endothelial cell leptin receptors, leptin and interleukin-8 in the pathogenesis of preeclampsia: An in-vitro study

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