Maternal Inflammation May Disrupt Infant Brain Wiring

Summary: A new research reveals that infection during pregnancy may affect neurodevelopment in infants by reducing CD11c-positive microglia—key immune cells that support mental myelination. These cells produce IGF-1, a proteins essential for forming the myelin sheath that helps muscle impulses travel quickly.

In both animals and preeclampsia babies exposed to parental infection, researchers found decreased amounts of IGF-1 and delayed neuroplasticity on MRI scans. The results suggest a potential therapeutic target to safeguard child mental development and reduce the long-term consequences of antenatal disease.

Important Information:

Important Cells Affected: Parental disease reduces CD11c-positive microglia during growth.
• Myelination Delays: Lower IGF-1 rates linked to disrupted nerve development in infants.
• Medical Potential: Targeting microglia perhaps prevent long-term developmental delays.

Origin: Nagoya University

A research team led by Nagoya University Graduate School of Medicine in Japan has uncovered a possible method linking maternal infection to delayed neurodevelopment in babies.

The study suggests the position of CD11c-positive microglia—immune cells in the brain essential for myelination—during child mental development.

The findings, published in&nbsp, Communications Biology, suggest new techniques to alleviate the long-term developmental effects of maternal infection. &nbsp,

Swelling during pregnancy occurs when the family’s immune system becomes activated during pregnancy, usually due to an infection, immune response, or economic factors. It can have negative results for the girl, probably causing long-term mental and behavioral challenges. &nbsp, &nbsp,

Then, a study group led by Kazuya Fuma and Tomomi Kotani has discovered the part of CD11c-positive microglia in this process. Microglia, the body’s immune tissues, play a vital role in neuroplasticity, the method where nerve fibers are coated with axons. Myelin is necessary for making the brain tissue able to transmit electrical impulses quickly. &nbsp, &nbsp,

Second, the scientists tested animals that were exposed to maternal disease. They found that the development of these organisms was reduced. Finally, to determine if these findings were related to humans, the researchers analyzed cable blood from premature infants exposed to chorioamnionitis, a condition that causes infection 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. &nbsp, &nbsp,

” 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” .&nbsp,

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. &nbsp, &nbsp,

” 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” .&nbsp,

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⁺&nbsp, microglia, key contributors to myelination through IGF-1 production, in this pathology. In the mouse model, the CD11c⁺&nbsp, 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⁺&nbsp, microglia during early development occurred similarly in mice and humans. Notably, a lack of high CD11c⁺&nbsp, microglial population has been observed in children with neurodevelopmental disorders.

This study reports impaired induction of CD11c⁺&nbsp, 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.