A groundbreaking study led by Nagoya University Graduate School of Medicine has unveiled a potential mechanism connecting maternal inflammation during pregnancy to delayed neurodevelopment in infants. The research, published in Communications Biology, highlights the critical role of CD11c-positive microglia, immune cells in the brain vital for myelination, during early brain development. The findings offer promising insights into strategies that could mitigate the long-term neurodevelopmental effects of maternal inflammation.
Inflammation during pregnancy can arise from various factors, such as infections, autoimmune responses, or environmental influences, and has been linked to negative outcomes for infants, including cognitive and behavioral challenges later in life.
The research team, led by Kazuya Fuma and Tomomi Kotani, focused on the role of CD11c-positive microglia—immune cells in the brain involved in myelination, a process where nerve fibers are coated with myelin, enabling efficient transmission of electrical signals between nerve cells. Their study reveals that maternal inflammation significantly impacts the proliferation of these cells, potentially contributing to delays in infant neurodevelopment.
In their initial tests, the researchers exposed mice to maternal inflammation and observed a reduction in the proliferation of CD11c-positive microglia. To determine the relevance of this finding to humans, the team analyzed cord blood from preterm infants who had been exposed to chorioamnionitis, an inflammation-related condition during pregnancy. The results showed lower levels of IGF-1, a protein associated with CD11c-positive microglia, in the infants’ samples. Furthermore, MRI scans revealed a higher incidence of delayed myelination in these infants.
Fuma explained, “Inflammation during pregnancy suppressed the increase in CD11c microglia that we typically observe during normal infant development. Since CD11c microglia are a major source of IGF-1, both were found to be diminished in the presence of maternal inflammation, indicating that this critical pathway is impaired in children with delayed neurodevelopment.”
The study underscores the complex relationship between maternal inflammation and infant brain development. With further research, the team hopes to identify therapeutic interventions that could protect infants from the long-term consequences of impaired myelination.
“If future studies confirm a reduction in these microglia in preterm infants exposed to inflammatory conditions like chorioamnionitis, early interventions may be developed to reduce or prevent neurodevelopmental delays,” Fuma stated. “Targeting CD11c-positive microglia could help protect infants from the lasting effects of impaired myelination, enhancing their potential for healthy cognitive development.”
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