Maternal immune response affects fetal brain development

Mia Brain Development Neuroscience


Summary: Immune responses during pregnancy can alter gene regulation in the brain of developing mouse embryos. Researchers have found that maternal immunity affects microglia, brain cells that surround neurons.

These changes persist in young mice, suggesting long-term effects on brain development. This research helps to understand the origins of neurodevelopmental disorders such as autism and schizophrenia.

Key facts:

  • The role of microgliaMaternal immune responses have been found in microglia in the fetal brain, which influence gene regulation.
  • Constant changes: Gene changes in the brain persist well into young adulthood, long after the immune response has declined.
  • Effects of neurodevelopmentThe findings provide insights into how maternal infections contribute to neurodevelopmental disorders.

Source: Company of Biologists

No parent wants to expose their child to a serious infection, especially while they are still in the womb, but they know they have immunity. Response Can a viral infection during pregnancy affect the development of the child in the womb?

Scientists at Harvard University in Cambridge, USA, have shown that the immune response in pregnant mice is detected by a specific brain cell in the developing fetus and changes how genes are ordered in the brain – a change that persists in young mice.

This Shows The Baby And Immune Cells.
Although most viral infections are usually short-lived, scientists have found that the changes that the mother’s immune system makes to the brain cells of the fetus continue well after the immune system has subsided. Credit: Neuroscience News

It was published in the magazine today DevelopmentThis research will help researchers understand how the mother’s immune response affects brain development in fetuses and the origins of neurodevelopmental disorders such as autism.

Scientists have long suspected that fetal exposure to infectious bugs increases the risk of developing neurological diseases such as schizophrenia and autism spectrum disorders.

There is evidence that fighting infection during pregnancy can affect the development of offspring in the womb, even if the embryos themselves are not infected.

However, it remains unclear how fetuses sense their parents’ immune responses and the exact consequences for their development.

In a recent study, a team led by Professor Paola Arlotta at Harvard University identified a specific type of cell in the mouse fetal brain that is responsible for the immune response to the mother.

The researchers used a virus-like compound to stimulate an immune response in pregnant mice without causing an actual infection. They then determined how cells in the fetal brain responded by evaluating which genes were turned on or off.

Using this approach, the scientists showed that cells called ‘microglia’ can sense the mother’s immune response.

“Microglia are immune cells of the brain. They play a critical role during inflammation and infection and have fundamental functions in healthy brain development,” Arlotta explained.

Following the mother’s immune response, the microglia of the fetus will change which genes are activated or activated, which also happens in the surrounding brain cells, such as neurons.

Interestingly, gene regulation changes in neighboring cells depend on microglia in the brain; When the researchers repeated the experiments using mice without microglia, other brain cells did not respond to the mother’s immune response.

Although most viral infections are usually short-lived, scientists have discovered that the changes that the mother’s immune system makes to the fetus’s brain cells persist well after the immune system has subsided.

“Based on previous studies showing that microglia exposed to early infections respond differently to stimuli in adults, we hypothesized that the maternal immune response would lead to changes in microglial genes that persist postnatally,” said study co-author Dr. Bridget Ostrem. .

This study advances our understanding of the cellular basis of neurodevelopmental disorders in humans.

“Our results suggest that microglia may be useful as therapeutic targets in the setting of maternal infections,” said Ostrem, although there is still much work to be done.

“Going forward, the changes we observed in this study will be critical in determining the long-term behavioral implications,” added Harvard researcher Dr. Nuria Domínguez-Iturza.

So maternal protection and fetal development research news

Author: Alex Eve
Source: Company of Biologists
Contact: Alex Eve – Company of Biologists
Image: Image credited to Neuroscience News.

Preliminary study: Open Access.
The fetal brain response to maternal inflammation requires microglia” by Ann Manning et al Development


Draft

The fetal brain response to maternal inflammation requires microglia

In the womb Infection and maternal inflammation can negatively affect fetal brain development. Maternal systemic disease, even in the absence of direct fetal brain infection, increases the risk of neuropsychiatric disorders in affected offspring.

The cell types involved in the fetal brain’s response to maternal inflammation are largely unknown, creating barriers to new therapeutic approaches.

Here, we show that microglia, the brain’s resident phagocytes, express receptors for pathogens and cytokines throughout early embryonic development.

Using a rat maternal immune activation (MIA) model in which polyinosinic:polycytidylic acid is injected into pregnant mice, we demonstrate long-term transcriptional changes in fetal microglia that persist throughout postnatal life.

We observe that MIA induces gene expression changes in neuronal and non-neuronal cells; Importantly, these responses are abrogated by a microglia-selective genetic deletion, indicating that microglia are required for other cortical cell types to respond to MyAIA transcription.

These findings demonstrate that microglia play an important and persistent role in the maternal inflammatory response in the fetus, and should be explored as potential therapeutic cell targets.

Exit mobile version