College of Nursing Martha S. Pitzer Center for Women, Children and Youth, The Ohio State University, Columbus, USA.
School of Nursing, University of Pittsburgh, Pittsburgh, USA.
Am J Reprod Immunol. 2023 Sep;90(3):e13763. doi: 10.1111/aji.13763.
Obesity and preeclampsia both involve a pathological inflammatory response, which may be how obesity increases preeclampsia risk. Previous studies have failed to assess robust measurements of inflammatory markers across gestation, specifically in overweight/ obese women in the context of preeclampsia.
We measured 20 inflammatory markers in plasma via multiplex assay (ThermoFisher Inflammation 20 plex Human ProcartaPlex Panel) across the three trimesters of pregnancy in an existing cohort of overweight and obese women who developed preeclampsia (n = 37) and without preeclampsia (n = 74). Mann-Whitney U tests examined differences in inflammatory marker concentrations between cases and controls. Repeated measures ANOVA tests were used to explore differences in inflammatory marker concentrations over time within cases and controls.
Pro-inflammatory markers (IL-1α, IL-1β, IL-6, IFN-α, IFN-γ, GM-CSF, IL-12p70, IL-17α, TNF-α, IL-8) and anti-inflammatory markers (IL-4, IL-10, IL-13) were higher in the first and second trimester in participants who later developed preeclampsia compared to those who did not (p < .05). Only TNF-α and IL-8 remained elevated in the third trimester. Inflammatory markers did not change across pregnancy in preeclampsia cases but did increase across pregnancy in controls.
Our findings diverge from prior studies, predominantly of non-obese women, that report lower circulating concentrations of anti-inflammatory cytokines in preeclampsia versus normotensive pregnancy, particularly by late pregnancy. We posit that women with overweight and obesity who develop preeclampsia entered pregnancy with a heightened pro-inflammatory state likely related to obesity, which increased risk for preeclampsia. Further studies are needed to investigate if inflammatory maker profiles differ between obese and non-obese women.
肥胖和子痫前期都涉及病理性炎症反应，这可能是肥胖增加子痫前期风险的原因。以前的研究未能在整个孕期评估炎症标志物的稳健测量值，特别是在超重/肥胖的子痫前期妇女中。
我们通过多重分析（ThermoFisher Inflammation 20 plex Human ProcartaPlex Panel）测量了现有超重和肥胖孕妇队列中 37 例子痫前期患者和 74 例无子痫前期患者妊娠的三个孕期中 20 种炎症标志物。Mann-Whitney U 检验比较了病例组和对照组炎症标志物浓度的差异。重复测量方差分析检验了病例组和对照组炎症标志物浓度随时间的变化。
与未发生子痫前期的孕妇相比，在发生子痫前期的孕妇中，第一和第二孕期的促炎标志物（IL-1α、IL-1β、IL-6、IFN-α、IFN-γ、GM-CSF、IL-12p70、IL-17α、TNF-α、IL-8）和抗炎标志物（IL-4、IL-10、IL-13）浓度更高（p<0.05）。只有 TNF-α和 IL-8 在第三孕期仍升高。子痫前期患者的炎症标志物在整个孕期没有变化，但对照组的炎症标志物随孕期增加而增加。
我们的研究结果与以前主要针对非肥胖妇女的研究结果不同，后者报告子痫前期与正常妊娠相比，循环中抗炎细胞因子的浓度较低，尤其是在妊娠晚期。我们认为，超重和肥胖的子痫前期患者在妊娠时处于较高的促炎状态，这可能与肥胖有关，增加了子痫前期的风险。需要进一步的研究来探讨肥胖和非肥胖妇女的炎症标志物谱是否存在差异。
