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Investigation of the effect of intrauterine inflammation and infection on fetal brain injury using human and animal models.

机译：使用人类和动物模型研究宫内炎症和感染对胎儿脑损伤的影响。

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In recent years, increased focus has been placed on the role of intrauterine infection and inflammation in the pathogenesis of fetal brain injury leading to neurodevelopmental disorders such as cerebral palsy. At present, the mechanisms by which inflammatory processes during pregnancy cause this effect on the fetus are poorly understood. Our previous work has indicated an association between experimentally-induced intrauterine infection, increased proinflammatory cytokines, and increased white matter injury in the guinea pig fetus. In order to further elucidate the pathways by which inflammation in the maternal system or the fetal membranes leads to fetal impairment, a number of studies investigating aspects of the disease process have been performed. These studies represent a body of work encompassing novel research and results in a number of human and animal studies.; Using a guinea pig model of inflammation, increased amniotic fluid proinflammatory cytokines and fetal brain injury were found after a maternal inflammatory response was initiated using endotoxin. In order to more closely monitor the fetal response to chorioamnionitis, a model using the chronically catheterized fetal ovine was carried out. This study demonstrated the adverse effects on fetal white matter after intrauterine exposure to bacterial inoculation, though the physiological parameters of the fetus were relatively stable throughout the experimental protocol, even when challenged with intermittent hypoxic episodes.; The placenta is an important mediator between mother and fetus during gestation, though its role in the inflammatory process is largely undefined. Studies on the placental role in the inflammatory process were undertaken, and the limited ability of proinflammatory cytokines and endotoxin to cross the placenta are detailed herein.; Neurodevelopmental disorders can be monitored in animal models in order to determine effective disease models for characterization of injury and use in therapeutic strategies. Our characterizations of postnatal behaviour in the guinea pig model using motility monitoring and spatial memory testing have shown small but significant differences in pups exposed to inflammatory processes in utero.; The data presented herein contributes a breadth of knowledge to the ongoing elucidation of the pathways by which fetal brain injury occurs. Determining the pathway of damage will lead to discovery of diagnostic criteria, while determining the vulnerabilities of the developing fetus is essential in formulating therapeutic options.
机译：近年来，越来越重视子宫内感染和炎症在胎儿脑损伤导致神经发育障碍（如脑瘫）的发病机理中的作用。目前，对怀孕期间炎症过程对胎儿造成这种影响的机制了解甚少。我们以前的工作表明实验性子宫内感染，豚鼠胎儿促炎性细胞因子增加和白质损伤增加之间存在关联。为了进一步阐明母体系统或胎儿膜炎症导致胎儿损伤的途径，已经进行了许多研究疾病过程方面的研究。这些研究代表了一项新颖的研究，并在许多人类和动物研究中取得了成果。使用豚鼠的炎症模型，使用内毒素引发母体炎症反应后，发现羊水促炎细胞因子和胎儿脑损伤增加。为了更紧密地监测胎儿对绒毛膜羊膜炎的反应，建立了使用慢性插管胎儿羊的模型。尽管胎儿的生理参数在整个实验方案中相对稳定，即使受到间歇性低氧发作的挑战，这项研究也证明了子宫内暴露于细菌接种后对胎儿白质的不利影响。尽管胎盘在炎症过程中的作用尚不清楚，但在妊娠期间胎盘是母亲与胎儿之间的重要介体。进行了关于胎盘在炎症过程中的作用的研究，并且本文详细描述了促炎细胞因子和内毒素穿过胎盘的有限能力。可以在动物模型中监测神经发育障碍，以确定用于表征损伤的有效疾病模型并用于治疗策略。我们通过运动监测和空间记忆测试对豚鼠模型中的产后行为进行了表征，结果表明，暴露于子宫内炎症过程的幼崽差异很小，但存在显着差异。本文提供的数据有助于不断阐明胎儿脑损伤的发生途径。确定损害的途径将导致发现诊断标准，而确定发育中的胎儿的脆弱性对制定治疗方案至关重要。

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