Hypoxic-ischemic brain injury remains a leading cause of mortality and morbidity in neonates. The inflammatory response, which is characterized in part by activation of local immune cells, has been implicated as a core component for the progression of damage to the immature brain following hypoxia-ischemia (HI). However, mounting evidence implicates circulating immune cells recruited to the site of damage as orchestrators of neuron-glial interactions and perpetuators of secondary brain injury. This suggests that re-directing our attention from the local inflammatory response toward the molecular mediators believed to link brain-immune cell interactions may be a more effective approach to mitigating the inflammatory sequelae of perinatal HI. In this review, we focus our attention on cyclooxygenase-2, a mediator by which peripheral immune cells may modulate signaling pathways in the brain that lead to a worsened outcome. Additionally, we present an overview of emerging therapeutic modalities that target mechanisms of neuroinflammation in the hypoxic-ischemic neonate. © 2011 Springer-Verlag/Wien.
CITATION STYLE
Fathali, N., Khatibi, N. H., Ostrowski, R. P., & Zhang, J. H. (2011). The evolving landscape of neuroinflammation after neonatal hypoxia-ischemia. In Acta Neurochirurgica, Supplementum (pp. 93–100). Springer-Verlag Wien. https://doi.org/10.1007/978-3-7091-0693-8_15
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