Malaria in pregnancy (MiP) induces intrauterine growth restriction (IUGR) and preterm labour (PTL). However, its effects on yolk sac morphology and function are largely unexplored. We hypothesized that MiP modifies yolk sac morphology and efflux transport potential by modulating ABC efflux transporters. C57BL/6 mice injected with Plasmodium berghei ANKA (5 × 10⁵ infected erythrocytes) at gestational day (GD) 13.5 were subjected to yolk sac membrane harvesting at GD 18.5 for histology, qPCR and immunohistochemistry. MiP did not alter the volumetric proportion of the yolk sac's histological components. However, it increased levels of Abcb1a mRNA (encoding P‐glycoprotein) and macrophage migration inhibitory factor (Mif chemokine), while decreasing Abcg1 (P < 0.05); without altering Abca1, Abcb1b, Abcg2, Snat1, Snat2, interleukin (Il)‐1β and C‐C Motif chemokine ligand 2 (Ccl2). Transcripts of Il‐6, chemokine (C‐X‐C motif) ligand 1 (Cxcl1), Glut1 and Snat4 were not detectible. ABCA1, ABCG1, breast cancer resistance protein (BCRP) and P‐gp were primarily immunolocalized to the cell membranes and cytoplasm of endodermic epithelium but also in the mesothelium and in the endothelium of mesodermic blood vessels. Intensity of P‐gp labelling was stronger in both endodermic epithelium and mesothelium, whereas ABCA1 labelling increased in the endothelium of the mesodermic blood vessels. The presence of ABC transporters in the yolk sac wall suggests that this fetal membrane acts as an important protective gestational barrier. Changes in ABCA1 and P‐gp in MiP may alter the biodistribution of toxic substances, xenobiotics, nutrients and immunological factors within the fetal compartment and participate in the pathogenesis of malaria‐induced IUGR and PTL.

中文翻译：

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妊娠疟疾调节小鼠内脏卵黄囊中的P-糖蛋白（P-gp / Abcb1a）和ABCA1外排转运蛋白。

妊娠疟疾（MiP）引起宫内生长受限（IUGR）和早产（PTL）。但是，其对卵黄囊形态和功能的影响尚待探索。我们假设MiP通过调节ABC外排转运蛋白来修饰卵黄囊形态和外排转运潜力。在妊娠日（GD）13.5注射了伯氏疟原虫ANKA（5×10 ⁵受感染的红细胞）的C57BL / 6小鼠接受卵黄囊膜收获，GD 18.5，用于组织学，qPCR和免疫组织化学。MiP不会改变卵黄囊组织学成分的体积比例。然而，它增加了Abcb1a mRNA（编码P-糖蛋白）和巨噬细胞迁移抑制因子（Mif趋化因子），同时降低Abcg1（P  <0.05）；而不改变Abca1，Abcb1b，Abcg2，Snat1，Snat2，白介素（II）-1β和C-C Motif趋化因子配体2（Ccl2）。的转录物IL-6 ，趋化因子（C-X-C基序）配体1（CXCL1），Glut1的和Snat4无法检测到。ABCA1，ABCG1，乳腺癌抗性蛋白（BCRP）和P-gp主要免疫定位在皮层上皮的细胞膜和细胞质上，但也免疫定位在皮层血管的间皮和内皮中。P-gp标记的强度在皮层上皮和间皮中均较强，而ABCA1标记在中皮血管的内皮中增加。卵黄囊壁中存在ABC转运蛋白，表明该胎膜可作为重要的妊娠保护屏障。MiP中ABCA1和P-gp的变化可能会改变胎儿室内有毒物质，异种生物，营养物质和免疫因素的生物分布，并参与疟疾诱发的IUGR和PTL的发病机制。