Tency I
Department of Obstetrics and Gynaecology, Faculty of Medicine and Health Sciences, Ghent University ; Department of Midwifery, Catholic University College HUB-KAHO, Sint-Niklaas.
Facts Views Vis Obgyn. 2014;6(1):19-30.
Preterm birth (PTB), defined as a delivery before 37 weeks of gestation, is the leading cause of perinatal morbidity and mortality worldwide. Diagnosis of preterm labour as well as accurate prediction of PTB is notoriously difficult. Preterm birth is initiated by multiple mechanisms including infection or inflammation which is the only pathological process for which a firm causal link with PTB has been established. Intrauterine infection evokes an immune response that involves the release of cytokines and chemokines, prostaglandins and matrix-degrading enzymes. These substances trigger uterine contractions, membrane rupture and cervical ripening. Most intra-uterine infections are chronic and subclinical in nature and consequently hard to diagnose before labour or rupture of the membranes. The best studied site of infection is amniotic fluid, but this requires an invasive procedure. A non-invasive approach seems to be more relevant to clinical practice. However, few studies have investigated the maternal inflammatory response during preterm labour. Therefore, the overall objective of this study was to determine several inflammatory markers in maternal serum from pregnant women in labour (either term or preterm) vs. non-labouring controls. We completed a nested case control study in which singleton pregnancies were recruited at Ghent University Hospital and divided into groups according to gestational age and labour status. Multiple proteins were evaluated in maternal serum using enzyme-linked or multiplex bead immunoassays including soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), matrix metalloproteinases (MMP)-9 and MMP-3, tissue inhibitor of metalloproteinases (TIMP)-1, TIMP-2, TIMP-3 and TIMP-4 and a panel of 30 cytokines, chemokines and growth factors.
早产（PTB）定义为妊娠37周前分娩，是全球围产期发病和死亡的主要原因。早产的诊断以及早产的准确预测非常困难。早产由多种机制引发，包括感染或炎症，这是唯一已确定与早产有明确因果关系的病理过程。宫内感染引发免疫反应，涉及细胞因子、趋化因子、前列腺素和基质降解酶的释放。这些物质引发子宫收缩、胎膜破裂和宫颈成熟。大多数宫内感染本质上是慢性和亚临床的，因此在分娩或胎膜破裂前很难诊断。研究最多的感染部位是羊水，但这需要侵入性操作。非侵入性方法似乎与临床实践更相关。然而，很少有研究调查早产期间的母体炎症反应。因此，本研究的总体目标是确定分娩孕妇（足月或早产）与未分娩对照组母体血清中的几种炎症标志物。我们完成了一项巢式病例对照研究，在根特大学医院招募单胎妊娠孕妇，并根据孕周和分娩状态分组。使用酶联或多重珠免疫测定法评估母体血清中的多种蛋白质，包括髓系细胞表达的可溶性触发受体-1（sTREM-1）、基质金属蛋白酶（MMP）-9和MMP-3、金属蛋白酶组织抑制剂（TIMP）-1、TIMP-2、TIMP-3和TIMP-4以及一组30种细胞因子、趋化因子和生长因子。
