Phagocytosis as a potential mechanism for microbial defense of mouse placental trophoblast cells
Phagocytosis as a potential mechanism for microbial defense of mouse placental trophoblast cells
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DOI：
10.1530/rep.1.00214
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发表时间：
2004-08-01
期刊：
影响因子：
3.8
通讯作者：
Bevilacqua, E
中科院分区：
文献类型：
--
作者：
Amarante-Paffaro, A;Queiroz, GS;Bevilacqua, E
滋养层巨细胞是着床期和着床后的活跃吞噬细胞。在胎盘成熟过程中，吞噬作用减少，因为营养的吞噬功能逐渐被迷路区滋养层对营养的直接摄取所取代。我们推测，胎盘成熟后，滋养层细胞保持吞噬功能的目的以外的营养。本研究采用组织学技术检查滋养层细胞吞噬微生物（酵母菌或细菌）的能力-在体内接受巯基乙酸盐激活巨噬细胞的女性和在体外存在吞噬促进剂（如干扰素-γ和补体成分C3）的情况下。妊娠后半期的胎盘滋养层细胞显示出基础吞噬作用，当将微生物接种到妊娠动物或引入培养系统中时，这些启动子可以显着上调。刺激的滋养层细胞吞噬的生物体更迅速，在更大的数量比非刺激的滋养层暴露于相同数量的生物体。两者合计，我们的研究结果表明，滋养层细胞不会失去他们的能力，吞噬在胎盘形成过程中，这可能意味着滋养层细胞参与胚胎和胎儿先天性免疫防御，通过消除微生物存在于母胎界面。
Trophoblast giant cells are active phagocytes during implantation and post-implantation. Phagocytosis decreases during placental maturation as the phagocytic function of nutrition is gradually replaced by the direct uptake of nutrients by the labyrinth zone trophoblast. We hypothesize that, after placental maturation, trophoblast cells maintain phagocytic functions for purposes other than nutrition. This study employs histological techniques to examine the ability of trophoblast cells to phagocytose microorganisms (yeast or bacteria) - in vivo in females receiving thioglycolate to activate macrophages and in vitro in the presence of phagocytic promoters such as interferon-gamma and complement component C3. Placental trophoblast cells from the second half of gestation show basal phagocytosis that can be dramatically up-regulated by these promoters when microorganisms are inoculated into pregnant animals or introduced into culture systems. Stimulated trophoblast cells phagocytosed organisms more rapidly and in greater numbers than non-stimulated trophoblast exposed to the same numbers of organisms. Taken together, our results indicate that trophoblast cells do not lose their ability to phagocytose during the placentation process, which may imply that trophoblast cells participate in embryonic and fetal innate immune defense through elimination of microorganisms present at the maternal-fetal interface.