A recent study published in Advanced Science News found that inflammation plays a key role in the development of brain injury following intraventricular hemorrhage (IVH), a potential complication of fetal and neonatal alloimmune thrombocytopenia (FNAIT).
Prior to this study, it was known that IVH can lead to neurodevelopmental damage in infants. However, the biochemical mechanism was not well-understood.
The authors developed a first-of-its-kind, three-dimensional model that mimics the environment of the human brain in a laboratory setting. This allowed them to discover that a molecule called interleukin-1B (IL1B) promotes inflammation in fetal nerve and brain cells, which may lead to brain injury.
“This innovative tool could significantly enhance our understanding of IVH-related pathology and facilitate the identification of potential therapeutic targets,” they wrote.
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In particular, the researchers investigated the subventricular zone of the brain, which is a major site of development after birth. IVH interferes with the normal functions of this zone by disrupting cellular growth and repair.
Findings revealed that when the model was exposed to red blood cells, a number of inflammatory and stress-related compounds became upregulated, including IL1B. Additionally, neural stem cell production decreased following exposure to red blood cells.
Next, the researchers exposed neural stem cells to newborn cerebrospinal fluid samples and again observed decreased cell growth, further supporting the role of IVH in causing neurodevelopmental damage. When treated with a drug that blocks IL1B, however, neural stem cell production was partially restored.
Together, these results highlight the potential of targeting IL1B to reduce the risk of neuronal injury among infants with FNAIT who develop IVH.
“This study advances the understanding of IVH and lays the groundwork for developing strategies to protect the developing brain,” the authors concluded.
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