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Maternal IL-10 restricts fetal emergency myelopoiesis [scATAC-seq]

GSE240914 Mus musculus Genome binding/occupancy profiling by high throughput sequencing 4 samples Submitted 2024/02/29 Platform GPL19057
Summary
We investigated how late fetal liver (FL) mouse hematopoieitic stem and progenitor cells (HSPC) respond to inflammation, with the hypothesis that deficits in engagement of emergency myelopoiesis (EM) pathways could limit neutrophil output and contribute to perinatal neutropenia, ultimately explaining the susceptibility of neonates to inflammation and infection. We show that fetal HSPCs are biased toward erythroid and lymphoid cell production at steady state and fail to mount classical EM responses in vivo. Despite being capable of responding to EM-inducing stimuli in vitro, we find that maternal factors like interleukin-10 (IL-10) restrict fetal HSPCs from activating EM pathways in utero. Accordingly, we find that loss of maternal IL-10 restores EM activation in fetal HSPCs but at a cost of premature parturition. These results reveal the evolutionary trade-off inherent in maternal anti-inflammatory responses that maintain pregnancy but render the fetus susceptible to infection.
Published in
Maternal inflammation regulates fetal emergency myelopoiesis
Collins A, Swann JW, Proven MA et al. · Cell 2024 · PMID 38428422 · doi:10.1016/j.cell.2024.02.002
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Also filed as BioProject PRJNA1005686 and SRA study SRP455264. Searching any of these in the dataset finder brings you back here.

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