Glucocorticosteroids Effects on Brain Development in the Preterm Infant: A Role for Microglia?

Prematurity, observed in 15 million births worldwide each year, is a clinical condition that is a major cause of neonatal mortality and morbidity in the short and long term. Preterm infants are at high risk of developing respiratory problems, sepsis, and other morbidities leading to neurodevelopment...

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Published inCurrent neuropharmacology Vol. 19; no. 12; pp. 2188 - 2204
Main Authors Manuela, Zinni, Julien, Pansiot, Elodie, Billion, Olivier, Baud, Jérôme, Mairesse
Format Journal Article
LanguageEnglish
Published United Arab Emirates Bentham Science Publishers Ltd 01.01.2021
Bentham Science Publishers
Subjects
Brain
Female
Humans
Infant Mortality
Infant, Newborn
Infant, Premature
Microglia
Neuroinflammatory Diseases
Pregnancy
brain development
Prematurity
neuroinflammation
prenatal
glucocorticosteroids
antenatal
microglia
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Summary:Prematurity, observed in 15 million births worldwide each year, is a clinical condition that is a major cause of neonatal mortality and morbidity in the short and long term. Preterm infants are at high risk of developing respiratory problems, sepsis, and other morbidities leading to neurodevelopmental impairment and neurobehavioral disorders. Perinatal glucocorticosteroids have been widely used for the prevention and treatment of adverse outcomes linked to prematurity. However, despite their short-term benefits due to their maturational properties, some clinical trials have shown an association between steroids exposure and abnormal brain development in infants born preterm. Neuroinflammation has emerged as a preeminent factor for brain injury in preterm infants, and the major role of microglia, the brain resident immune cells, has been recently highlighted. Considering the role of microglia in the modulation of brain development, the aim of this review is to summarize the effects of endogenous and exogenous glucocorticosteroids on brain development and discuss the possible role of microglia as the mediator of these effects.
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These authors contributed equally to this work
ISSN:1570-159X
1875-6190
DOI:10.2174/1570159X19666210517112913