Summary: A new study reveals that inflammation during pregnancy can affect neurological development in babies by reducing positive CD11c microglia: key immune cells that support myelinization of the brain. These cells produce IGF-1, a critical protein to form the myelin sheath that helps nerve signals to travel efficiently.
In both mice and premature babies exposed to maternal inflammation, researchers found decreased levels of IGF-1 and late myelinization in magnetic resonance explorations. The findings suggest a potential therapeutic objective to protect the development of the child brain and reduce the long -term effects of prenatal inflammation.
Key facts:
Critical cells affected: maternal inflammation reduces CD11c’s positive microglia during development. Mixture delays: lower levels of IGF-1 linked to myelin formation interrupted in babies.
Source: University of Nagoya
A research group led by the Faculty of Medicine of the University of Nagoya in Japan has discovered a potential mechanism that links maternal inflammation with the late task of neurodevelopment in babies.
The research suggests the role of positive microglia for CD11c (immune cells in the crucial brain for myelinization), the development of the child brain.
The results, published in Communications Biology, suggest new strategies to mitigate the effects of long -term neurodevelopmental development of maternal inflammation.
Inflammation during pregnancy occurs when the mother’s immune system is activated during pregnancy, usually due to an infection, autoimmune response or environmental factors. It can have negative results for the baby, which can cause cognitive and behavioral long -term challenges.
Now, a research team led by Kazuya smokes and Tomomi Kotani has discovered the role of positive CD11c microglia in this process. Microglia, the immune cells of the brain, play a key role in myelinization, the process where nerve fibers are coated with myelin. Myelin is essential to make nerve cells to transmit electrical signals efficiently.
First, the researchers tested mice that were exposed to maternal inflammation. They discovered that the proliferation of these cells was reduced. Then, to determine if these findings were relevant to humans, the researchers analyzed the blood of the umbilical cord of premature babies exposed to quorioamnionitis, a condition that causes inflammation during pregnancy.
They found lower levels of IGF-1, a protein linked to positive microglia for CD11c, in their samples. When they performed a magnetic resonance of babies, the scanning confirmed that they had a greater incidence of delayed myelinization.
“Inflammation during pregnancy suppressed the increase in CD11C microglyia that we generally see during the typical babies development,” he said.
“It has been reported that the CD11C microglia is involved in myelinization as it is an important source of IGF-1. In the present study, both decreased in inflammation during pregnancy, which suggests that this route is affected in children with retarded neuros development.”
This study sheds light on the complex relationship between maternal inflammation and neurodevelopment. Researchers hope that understanding the role of positive microglia for CD11c in neurological development leads to new therapeutic strategies.
“If future studies confirm a decrease in these microglia in premature babies exposed to inflammatory conditions, such as quorioamnionitis, early interventions could be developed to prevent or reduce the neurodevelopment impact of maternal inflammation,” said smokes.
“When addressing positive CD11c microglyia, it may be possible to protect babies from the long -term consequences of deteriorated honeyination and improve their possibilities of healthy cognitive development.”
On this news of maternal inflammation and neurodevelopment research
Author: Matthew Coslett
Source: University of Nagoya
Contact: Matthew Coslett – University of Nagoya
Image: The image is accredited to Neuroscience News
Original research: open access.
“Prenatal inflammation harms the early induction of positive CD1C microglyia and delays myelinization in neurological development disorders” by Kazuya smokes et al. Communications biology
Abstract
Prenatal inflammation harms the early induction of CD11c microglyia and delays honeyinization in neurological development disorders
Histological chorioamnionitis (HCA) is a form of maternal immune activation (MIA) linked to an increased risk of neurodevelopment disorders in offspring.
Our previous study identified neurological development alterations in a MIA mouse model that mimics HCA.
Therefore, this study investigated the role of CD11c+microglia, key taxpayers to myelinization through the production of IGF-1, in this pathology. In the mouse model, the CD11C+ microglial population was significantly lower in the MIA group than in the control group on the postnatal day (PN3D).
In addition, myelinization -related protein levels decreased significantly in the MIA group in PN8D. In humans, premature babies with HCA exhibited higher levels of IL-6 and IL-17A cord serum and lower levels of IGF-1 than those who do not have HCA, followed by a greater incidence of delayed myelinization in magnetic resonance at the term measurement age.
In silico analysis revealed that the transient induction of the CD11c+ microglyia during early development occurred similarly in mice and humans. In particular, the lack of a high CD11C+ microglial population has been observed in children with neurodevelopmental disorders.
This study informs the deteriorated induction of CD11c+ microglia during postnatal development in a MIA mouse model associated with late myelinization.
Our findings can inform strategies to improve results in Babies with HCA.
