An Immune Cell Could Explain How Maternal Inflammation Causes a Neurodevelopmental Disorder

A research group led by Nagoya University Graduate School of Medicine in Japan has uncovered a possible mechanism linking maternal inflammation and delayed neurodevelopment in infants. The research findings point to the role of CD11c-positive microglia – immune cells in the brain that are crucial for myelination – during infant brain development. The findings, published in Communications Biology, suggest new strategies for mitigating the long-term effects of maternal inflammation on neurodevelopment.

Researchers Analyze Cord Blood of Premature Babies

Inflammation during pregnancy occurs when the mother’s immune system is activated during gestation, typically due to infection, autoimmune response or environmental factors. This can have negative consequences for the baby and potentially lead to long-term cognitive and behavioral problems. Now, a research team led by Kazuya Fuma and Tomomi Kotani has discovered the role of CD11c-positive microglia in this process. Microglia, the immune cells of the brain, play a key role in myelination, the process by which nerve fibers are wrapped in myelin. Myelin is essential for nerve cells to transmit electrical signals efficiently.

Initially, the researchers tested mice exposed to maternal inflammation. They found that the proliferation of these cells was reduced. To determine whether these results are relevant to humans, the researchers then analyzed umbilical cord blood from premature babies exposed to chorioamnionitis, a condition that causes inflammation during pregnancy. They found lower levels of IGF-1, a protein associated with CD11c-positive microglia, in their samples. When the infants underwent MRI scans, the scans confirmed that they had a higher incidence of delayed myelination.

How Maternal Inflammation is Linked to the Baby’s Neurological Development

“The inflammation during pregnancy suppressed the increase in CD11c microglia that we normally 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 reduced during pregnancy due to inflammation, suggesting that this signaling pathway is impaired in children with delayed neurological development.” This study sheds light on the complex relationship between maternal inflammation and neurodevelopment.

The researchers hope that understanding the role of CD11c+ microglia in neurodevelopment will lead to new therapeutic strategies. If future studies confirm a decrease in these microglia in preterm infants exposed to inflammatory diseases such as chorioamnionitis, early interventions could be developed to prevent or reduce the effects of maternal inflammation on neurodevelopment. Targeting CD11c+ microglia may protect infants from the long-term consequences of impaired myelination and improve their chances of healthy cognitive development.