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White matter damage after chronic subclinical inflammation in newborn mice
Xiaoyang Wang1, Gunnel Hellgren, Chatarina Löfqvist
1Perinatal Center, Department of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, S-405 30 Gothenburg, Sweden. xiaoyang.wang@fysiologi.gu.se
Insights
Chronic inflammation in early life, even at subclinical levels, can impair brain development in preterm infants. This may lead to white matter injury and is linked to lower insulin-like growth factor 1 levels.
Area of Science:
- Neuroscience
- Developmental Biology
- Immunology
Background:
- Preterm infants exposed to inflammation face higher risks of white matter injury and cerebral palsy.
- Chronic inflammation's impact on developing white matter requires further investigation.
Purpose of the Study:
- To investigate the effects of chronic low-dose inflammation on developing white matter in a preclinical model.
- To assess changes in white matter, gray matter volume, and key growth factors.
Main Methods:
- Administered low-dose lipopolysaccharide (LPS) daily from postnatal days 3-11.
- Examined white matter integrity using immunohistochemistry for axonal, myelin, and oligodendrocyte markers at postnatal day 12.
- Measured serum levels of insulin-like growth factor 1 (IGF-1) and insulin-like factor binding protein-3 (IGFBP-3).
Main Results:
- LPS exposure reduced serum IGF-1 levels but not IGFBP-3.
- Impaired myelination was observed in the subcortical white matter at postnatal day 12.
- Decreased brain gray matter volume and increased spleen and liver weights were noted.
Conclusions:
- Chronic subclinical inflammation negatively impacts white and gray matter development in early life.
- The observed effects may be associated with a deficiency in insulin-like growth factor 1.
- Findings highlight the vulnerability of the developing brain to inflammatory insults.
Abstract:
Preterm infants exposed to inflammation are at increased risk of white matter injury and/or cerebral palsy. To investigate the effect of chronic inflammation on the developing white matter, we administered low-dose lipopolysaccharide once a day from postnatal days 3 to 11, examined white matter changes at postnatal day 12, and monitored serum levels of insulin-like growth factor 1 and insulin-like factor binding protein-3. A single injection of lipopolysaccharide decreased the serum insulin-like growth factor 1 level but not the insulin-like factor binding protein-3 level. At postnatal day 12, quantification of immunohistochemical staining for axonal, myelin, and oligodendrocyte markers revealed impaired myelination in subcortical white matter. In addition, brain gray matter volume decreased and spleen and liver weight increased at postnatal day 12. These data suggest chronic subclinical inflammation hampers development of white and gray matter in early life, which may be associated with insulin-like growth factor 1 deficiency.
