Summary: A new study reveals that inflammation during pregnancy may impair neurodevelopment in infants by reducing CD11c-positive microglia—key immune cells that support brain myelination. These cells produce IGF-1, a protein critical for forming the myelin sheath that helps nerve signals travel efficiently.
In both mice and preterm infants exposed to maternal inflammation, researchers found decreased levels of IGF-1 and delayed myelination on MRI scans. The findings suggest a potential therapeutic target to protect infant brain development and reduce the long-term effects of prenatal inflammation.
Key Facts:
- Critical Cells Affected: Maternal inflammation reduces CD11c-positive microglia during development.
- Myelination Delays: Lower IGF-1 levels linked to disrupted myelin formation in infants.
- Therapeutic Potential: Targeting microglia may prevent long-term neurodevelopmental delays.
Source: Nagoya University
A research group led by Nagoya University Graduate School of Medicine in Japan has uncovered a potential mechanism linking maternal inflammation to delayed neurodevelopment in infants.
The research suggests the role of CD11c-positive microglia—immune cells in the brain crucial for myelination—during infant brain development.
The results, published in Communications Biology, suggest new strategies to mitigate the long-term neurodevelopmental effects of maternal inflammation.
Inflammation during pregnancy occurs when the mother’s immune system becomes activated during pregnancy, typically due to an infection, autoimmune response, or environmental factors. It can have negative outcomes for the baby, potentially causing long-term cognitive and behavioral challenges.
Now, a research team led by Kazuya Fuma and Tomomi Kotani has discovered the role of CD11c-positive microglia in this process. Microglia, the brain’s immune cells, play a key role in myelination, the process where nerve fibers are coated with myelin. Myelin is essential for making the nerve cells able to transmit electrical signals efficiently.
First, the researchers tested mice that were exposed to maternal inflammation. They found that the proliferation of these cells was reduced. Then, to determine if these findings were relevant to humans, the researchers analyzed cord blood from preterm infants exposed to chorioamnionitis, a condition that causes inflammation during pregnancy.
They found lower levels of IGF-1, a protein linked to CD11c-positive microglia, in their samples. When they performed MRI of the infants, the scans confirmed that they had a higher incidence of delayed myelination.
“Inflammation during pregnancy suppressed the increase in CD11c microglia that we usually see during typical infant development,” Fuma said.
“CD11c microglia have been reported to be involved in myelination by being a major source of IGF-1. In the present study, both were decreased in inflammation during pregnancy, suggesting that this pathway is impaired in children with delayed neurodevelopment.”
This study sheds light on the complex relationship between maternal inflammation and neurodevelopment. The researchers hope that understanding the role of CD11c-positive microglia in neurodevelopment will lead to new therapeutic strategies.
“If future studies confirm a decrease in these microglia in preterm infants exposed to inflammatory conditions, such as chorioamnionitis, early interventions could be developed to prevent or reduce the neurodevelopmental impact of maternal inflammation,” Fuma said.
“By targeting CD11c-positive microglia, it may be possible to protect infants from the long-term consequences of impaired myelination and improve their chances for healthy cognitive development.”
About this maternal inflammation and neurodevelopment research news
Author: Matthew Coslett
Source: Nagoya University
Contact: Matthew Coslett – Nagoya University
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Prenatal Inflammation Impairs Early CD11c-Positive Microglia Induction and Delays Myelination in Neurodevelopmental Disorders” by Kazuya Fuma et al. Communications Biology
Abstract
Prenatal Inflammation Impairs Early CD11c-Positive Microglia Induction and Delays Myelination in Neurodevelopmental Disorders
Histological chorioamnionitis (HCA) is a form of maternal immune activation (MIA) linked to an increased risk of neurodevelopmental disorders in offspring.
Our previous study identified neurodevelopmental impairments in an MIA mouse model mimicking HCA.
Thus, this study investigated the role of CD11c+ microglia, key contributors to myelination through IGF-1 production, in this pathology. In the mouse model, the CD11c+ microglial population was significantly lower in the MIA group than in the control group on postnatal day 3 (PN3d).
Furthermore, myelination-related protein levels significantly decreased in the MIA group at PN8d. In humans, preterm infants with HCA exhibited higher IL-6 and IL-17A cord-serum levels and lower IGF-1 levels than those without HCA, followed by a higher incidence of delayed myelination on magnetic resonance imaging at the term-equivalent age.
In silico analysis revealed that the transient induction of CD11c+ microglia during early development occurred similarly in mice and humans. Notably, a lack of high CD11c+ microglial population has been observed in children with neurodevelopmental disorders.
This study reports impaired induction of CD11c+ microglia during postnatal development in a mouse model of MIA associated with delayed myelination.
Our findings may inform strategies for improving outcomes in infants with HCA.
