Center for Nanomedicine, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
Department of Chemical and Biomolecular Engineering, Johns Hopkins University, Baltimore, MD 21218, USA.
Sci Transl Med. 2021 Jan 13;13(576). doi: 10.1126/scitranslmed.abc6245.
Inflammation contributes to nearly 4 million global premature births annually. Here, we used a mouse model of intrauterine inflammation to test clinically used formulations, as well as engineered nanoformulations, for the prevention of preterm birth (PTB). We observed that neither systemic 17a-hydroxyprogesterone caproate (Makena) nor vaginal progesterone gel (Crinone) was sufficient to prevent inflammation-induced PTB, consistent with recent clinical trial failures. However, we found that vaginal delivery of mucoinert nanosuspensions of histone deacetylase (HDAC) inhibitors, in some cases with the addition of progesterone, prevented PTB and resulted in delivery of live pups exhibiting neurotypical development. In human myometrial cells in vitro, the P4/HDAC inhibitor combination both inhibited cell contractility and promoted the anti-inflammatory action of P4 by increasing progesterone receptor B stability. Here, we demonstrate the use of vaginally delivered drugs to prevent intrauterine inflammation-induced PTB resulting in the birth of live offspring in a preclinical animal model.
炎症导致全球每年近 400 万例早产。在这里,我们使用宫内炎症的小鼠模型来测试临床使用的制剂,以及工程纳米制剂,以预防早产 (PTB)。我们观察到,无论是全身性 17a-羟基孕酮己酸酯(Makena)还是阴道孕酮凝胶(Crinone)都不足以预防炎症引起的 PTB,这与最近的临床试验失败一致。然而,我们发现阴道给予组蛋白去乙酰化酶 (HDAC)抑制剂的 mucoinert 纳米混悬剂,在某些情况下添加孕酮,可以预防 PTB,并导致分娩出具有神经典型发育的活幼崽。在体外人子宫平滑肌细胞中,P4/HDAC 抑制剂联合抑制细胞收缩,并通过增加孕酮受体 B 的稳定性来促进 P4 的抗炎作用。在这里,我们证明了使用阴道给予的药物来预防宫内炎症引起的 PTB,从而在临床前动物模型中分娩出活的后代。