Bacterial infection alters placental ABC transporters expression. These transporters provide fetal protection against circulating xenobiotics and environmental toxins present in maternal blood. We hypothesized that lipopolysaccharide (LPS-bacterial mimic) alters the yolk sac morphology and expression of key ABC transporters in a gestational-age dependent manner. Yolk sac samples from C57BL/6 mice were obtained at gestational ages (GD) 15.5 and GD18.5, 4 or 24 hours after LPS exposure (150ug/kg; n = 8/group). Samples underwent morphometrical, qPCR and immunohistochemistry analysis. The volumetric proportions of the histological components of the yolk sac did not change in response to LPS. LPS increased Abcg2 expression at GD15.5, after 4 h of treatment (p < 0.05). No changes in Abca1, Abcb1a/b, Abcg1, Glut1, Snat1, Il-1β, Ccl2 and Mif were observed. Il-6 and Cxcl1 were undetectable in the yolk sac throughout pregnancy. Abca1, breast cancer resistance protein (Bcrp, encoded by Abcg2) and P-glycoprotein (P-gp/ Abcb1a/b) were localized in the endodermal (uterine-facing) epithelium and to a lesser extent in the mesothelium (amnion-facing), whereas Abca1 was also localized to the endothelium of the yolk sac blood vessels. LPS increased the labeling area and intensity of Bcrp in the yolk sac’s mesothelial cells at GD15.5 (4 h), whereas at GD18.5, the area of Bcrp labeling in the mesothelium (4 and 24 h) was decreased (p < 0.05). Bacterial infection has the potential to change yolk sac barrier function by affecting Bcrp and Abcg2 expression in a gestational-age dependent-manner. These changes may alter fetal exposure to xenobiotics and toxic substances present in the maternal circulation and in the uterine cavity.

细菌感染改变胎盘 ABC 转运蛋白的表达。这些转运蛋白为胎儿提供保护，使其免受母体血液中存在的循环外源性物质和环境毒素的影响。我们假设脂多糖（LPS-细菌模拟物）以孕龄依赖性方式改变卵黄囊形态和关键 ABC 转运蛋白的表达。 C57BL/6 小鼠的卵黄囊样本是在胎龄 (GD) 15.5 和 GD18.5、LPS 暴露（150ug/kg；n = 8/组）后 4 或 24 小时获得的。对样品进行形态测定、qPCR 和免疫组织化学分析。卵黄囊组织学成分的体积比例并未因脂多糖而改变。处理 4 小时后，LPS 在 GD15.5 时增加Abcg2表达 (p < 0.05)。未观察到Abca1、Abcb1a/b、Abcg1、Glut1、Snat1、Il-1β、Ccl2和Mif的变化。整个怀孕期间卵黄囊中检测不到Il-6和Cxcl1 。 Abca1、乳腺癌耐药蛋白（Bcrp，由Abcg2编码）和 P-糖蛋白 (P-gp/ Abcb1a/b)定位于内胚层（面向子宫）上皮，并在较小程度上定位于间皮（面向羊膜） ，而 Abca1 也定位于卵黄囊血管的内皮细胞。 LPS 增加了 GD15.5（4 小时）卵黄囊间皮细胞中 Bcrp 标记面积和强度，而在 GD18.5 时，间皮细胞（4 和 24 小时）中 Bcrp 标记面积减少（p < 0.05） ）。细菌感染有可能以孕龄依赖性方式影响 Bcrp 和Abcg2 的表达，从而改变卵黄囊屏障功能。 这些变化可能会改变胎儿对母体循环和子宫腔中存在的异生物质和有毒物质的暴露。