Molvarec Attila, Czegle Ibolya, Szijártó János, Rigó János
First Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary.
Third Department of Internal Medicine, Semmelweis University, Budapest, Hungary.
J Reprod Immunol. 2015 Nov;112:53-7. doi: 10.1016/j.jri.2015.05.007. Epub 2015 Jun 23.
Increasing evidence suggests that an exaggerated maternal systemic inflammatory response and an angiogenic imbalance might play a central role in the pathogenesis of preeclampsia. We determined circulating levels of interleukin-17 (IL-17) along with those of angiogenic factors in healthy nonpregnant and pregnant women and preeclamptic patients, and examined whether serum IL-17 levels of preeclamptic patients were related to their clinical features and angiogenic factor concentrations. Fifty-nine preeclamptic patients, 60 healthy pregnant women and 56 healthy nonpregnant women were involved in this case-control study. Serum levels of IL-17A were measured using a high-sensitivity ELISA. Serum total soluble fms-like tyrosine kinase-1 (sFlt-1) and biologically active placental growth factor (PlGF) levels were determined by electrochemiluminescence immunoassay. For statistical analyses, nonparametric methods were applied. Serum IL-17 levels were significantly higher in preeclamptic patients than in healthy nonpregnant and pregnant women. We did not find any relationship between serum IL-17 concentrations of preeclamptic patients and their clinical features and serum sFlt-1 and PlGF levels or sFlt-1/PlGF ratios. However, elevated serum IL-17 level and sFlt-1/PlGF ratio were found to have an additive effect on the risk of preeclampsia, as shown by the substantially higher odds ratios of a combination of the two than of either alone. In conclusion, serum IL-17 levels are increased in preeclampsia, which may contribute to the development of the excessive systemic inflammatory response characteristic of the maternal syndrome of the disease. In addition, elevated serum IL-17 level and sFlt-1/PlGF ratio had an additive (joint) effect on the risk of preeclampsia.
越来越多的证据表明，母体全身炎症反应过度和血管生成失衡可能在先兆子痫的发病机制中起核心作用。我们测定了健康非孕妇、孕妇和先兆子痫患者循环中的白细胞介素-17（IL-17）水平以及血管生成因子水平，并研究了先兆子痫患者的血清IL-17水平是否与其临床特征以及血管生成因子浓度相关。59例先兆子痫患者、60例健康孕妇和56例健康非孕妇参与了这项病例对照研究。采用高灵敏度酶联免疫吸附测定法测量血清IL-17A水平。通过电化学发光免疫测定法测定血清总可溶性fms样酪氨酸激酶-1（sFlt-1）和生物活性胎盘生长因子（PlGF）水平。进行统计分析时采用非参数方法。先兆子痫患者的血清IL-17水平显著高于健康非孕妇和孕妇。我们未发现先兆子痫患者的血清IL-17浓度与其临床特征、血清sFlt-1和PlGF水平或sFlt-1/PlGF比值之间存在任何关系。然而，发现血清IL-17水平升高和sFlt-1/PlGF比值对先兆子痫风险具有相加作用，两者联合时的优势比远高于单独一项升高时的优势比。总之，先兆子痫患者血清IL-17水平升高，这可能有助于该疾病母体综合征特征性的过度全身炎症反应的发展。此外，血清IL-17水平升高和sFlt-1/PlGF比值对先兆子痫风险具有相加（联合）作用。
