Pulmonary maternal immune activation does not cross the placenta but leads to fetal metabolic adaptation

母体肺部免疫激活不会穿过胎盘,但会导致胎儿代谢适应

阅读:8
作者:Signe Schmidt Kjølner Hansen, Robert Krautz #, Daria Rago #, Jesper Havelund, Arnaud Stigliani, Nils J Færgeman, Audrey Prézelin, Julie Rivière, Anne Couturier-Tarrade, Vyacheslav Akimov, Blagoy Blagoev, Betina Elfving, Ditte Neess, Ulla Vogel, Konstantin Khodosevich, Karin Sørig Hougaard, Albin San

Abstract

The fetal development of organs and functions is vulnerable to perturbation by maternal inflammation which may increase susceptibility to disorders after birth. Because it is not well understood how the placenta and fetus respond to acute lung- inflammation, we characterize the response to maternal pulmonary lipopolysaccharide exposure across 24 h in maternal and fetal organs using multi-omics, imaging and integrative analyses. Unlike maternal organs, which mount strong inflammatory immune responses, the placenta upregulates immuno-modulatory genes, in particular the IL-6 signaling suppressor Socs3. Similarly, we observe no immune response in the fetal liver, which instead displays metabolic changes, including increases in lipids containing docosahexaenoic acid, crucial for fetal brain development. The maternal liver and plasma display similar metabolic alterations, potentially increasing bioavailability of docosahexaenoic acid for the mother and fetus. Thus, our integrated temporal analysis shows that systemic inflammation in the mother leads to a metabolic perturbation in the fetus.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。