Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock


Placental dysfunction influences fetal monocyte subpopulation gene expression in preterm birth.


The placenta is the primary organ for immune regulation, nutrient delivery, gas exchange, protection against environmental toxins, and physiologic perturbations during pregnancy. Placental inflammation and vascular dysfunction during pregnancy are associated with a growing list of prematurity-related complications. The goal of this study was to identify differences in gene expression profiles in fetal monocytes - cells that persist and differentiate postnatally - according to distinct placental histologic domains. Here, by using bulk RNA sequencing (RNA-Seq), we report that placental lesions are associated with gene expression changes in fetal monocyte subsets. Specifically, we found that fetal monocytes exposed to acute placental inflammation upregulate biological processes related to monocyte activation, monocyte chemotaxis, and platelet function while monocytes exposed to maternal vascular malperfusion lesions downregulate these processes. Additionally, we show that intermediate monocytes might be a source of mitogens, such as HBEGF, NRG1, and VEGFA, implicated in different outcomes related to prematurity. This is the first study to show that placental lesions are associated with unique changes in fetal monocytes and monocyte subsets. As fetal monocytes persist and differentiate into various phagocytic cells following birth, our study may provide insight into morbidity related to prematurity and ultimately potential therapeutic targets.

Authors: Sharma AM, Birkett R, Lin ET, Ernst LM, Grobman WA, Swaminathan S, Abdala-Valencia H, Misharin AV, Bartom ET, Mestan KK,
Journal: JCI Insight;2022Apr26. doi:10.1172/jci.insight.155482
Year: 2022
PubMed: PMID: 35471950 (Go to PubMed)