Neuroinflammation and neuroimmune dysregulation after acute hypoxic-ischemic injury of developing brain

Research output: Contribution to journalReview article

Abstract

Hypoxic-ischemic (HI) injury to developing brain results from birth asphyxia in neonates and from cardiac arrest in infants and children. It is associated with varying degrees of neurologic sequelae, depending upon the severity and length of HI. Global HI triggers a series of cellular and biochemical pathways that lead to neuronal injury. One of the key cellular pathways of neuronal injury is inflammation. The inflammatory cascade comprises activation and migration of microglia - the so-called "brain macrophages," infiltration of peripheral macrophages into the brain, and release of cytotoxic and proinflammatory cytokines. In this article, we review the inflammatory and immune mechanisms of secondary neuronal injury after global HI injury to developing brain. Specifically, we highlight the current literature on microglial activation in relation to neuronal injury, proinflammatory and anti-inflammatory/restorative pathways, the role of peripheral immune cells, and the potential use of immunomodulators as neuroprotective compounds.

Original languageEnglish (US)
Article number144
JournalFrontiers in Pediatrics
Volume2
Issue numberJAN
DOIs
StatePublished - Jan 1 2015

Fingerprint

Brain Injuries
Wounds and Injuries
Brain
Macrophages
Asphyxia
Immunologic Factors
Microglia
Heart Arrest
Nervous System
Anti-Inflammatory Agents
Parturition
Newborn Infant
Cytokines
Inflammation

Keywords

  • Developing brain
  • Hypoxia-ischemic encephalopathy
  • Immune dysregulation
  • Inflammation
  • Microglia

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

Cite this

Neuroinflammation and neuroimmune dysregulation after acute hypoxic-ischemic injury of developing brain. / Bhalala, Utpal S.; Koehler, Raymond C; Kannan, Sujatha.

In: Frontiers in Pediatrics, Vol. 2, No. JAN, 144, 01.01.2015.

Research output: Contribution to journalReview article

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