Summary of Study ST003130
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001943. The data can be accessed directly via it's Project DOI: 10.21228/M8K43P This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
Study ID | ST003130 |
Study Title | Pulmonary maternal immune activation does not extend through the placenta but leads to fetal metabolic adaptation - Maternal blood |
Study Summary | Maternal immune system activation (MIA) during pregnancy can disrupt the fetal environment, causing postnatal susceptibility to disorders. How the placenta and the fetus respond to acute MIA over time is unknown. Here, we characterized the response to acute maternal pulmonary inflammation across time in maternal and fetal organs using multi-omics. Unlike maternal organs which mounted strong innate immune responses, the placenta upregulated tissue-integrity genes, likely to prevent fetal exposure to infections, and downregulated growth-associated genes. Subsequently, the placenta upregulated biosynthesis and endoplasmic reticulum stress genes in order to return to homeostasis. These responses likely protected the fetus, since we observed no immune response in fetal liver. Instead, likely due to nutrient depletion, the fetal liver displayed metabolic adaptations, including increases in lipids containing docosahexaenoic acid, crucial for fetal brain development. Our study shows, for the first time, the integrated temporal response to pulmonary MIA across maternal and fetal organs. |
Institute | University of Copenhagen |
Department | Department of Biology |
Laboratory | Section for Computational and RNA Biology |
Last Name | Sandelin |
First Name | Albin |
Address | Copenhagen University Ole Maaloes Vej 5, DK2200, Copenhagen N, Denmark |
albin@binf.ku.dk | |
Phone | +45 224 56668 |
Submit Date | 2024-03-12 |
Raw Data Available | Yes |
Raw Data File Type(s) | mzML |
Analysis Type Detail | LC-MS |
Release Date | 2024-04-02 |
Release Version | 1 |
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Treatment:
Treatment ID: | TR003256 |
Treatment Summary: | Lipopolysaccharide (LPS; E. Coli serotype 00:55 B5 LPS (Sigma Lot nr. 025M4040V)) was diluted to the final concentration (0.02 µg/µl) in double distilled pyrogen-free water (Chem-Lab, Zedelgem, Belgium). In the morning of GD 17, the pregnant mice were semi-randomized into control and LPS treatment groups (denoted Ctrl and LPS, respectively), evenly distributing weights among the groups. Out of 80 mice in total, 74 were pregnant. Animals were placed in a whole-body inhalation chamber with an attached anaesthetic vaporizer (Penlon Sigma Delta, Abingdon, UK), delivering 3-4% isoflurane in filtered air, and were intratracheally instilled with 50 µl of vehicle (Ctrl) or 1 μg LPS in 50 µl vehicle, followed by 200μl of air. Vehicle and LPS were administered through a 0.58 mm polyethylene tube (Ref: 427411, Becton Dickinson, Brøndby, Denmark) attached to a plastic syringe. The procedure has been shown not to affect gestation, offspring viability nor growth75. After instillation, animals were returned to their cage, briefly placed on heating pads and checked upon regularly until euthanization |