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Related Concept Videos

Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...

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Related Experiment Video

Updated: Jul 26, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

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Neonatal Encephalopathy Is Associated With Altered IL-8 and GM-CSF Which Correlates With Outcomes.

Deirdre U Sweetman1,2,3, Tammy Strickland4,5, Ashanty M Melo4,5

  • 1Neonatology, National Maternity Hospital, Dublin, Ireland.

Frontiers in Pediatrics
|February 25, 2021
PubMed
Summary

Elevated Interleukin-8 (IL-8) and Granulocyte-Macrophage-Colony-Stimulating-Factor (GM-CSF) in newborns with NE correlate with brain injury and poor outcomes. These cytokines may predict NE severity and long-term neurodevelopmental deficits.

Keywords:
cytokineshypoxic-ischemic encephalopathyneonatal brain injuryoutcomesperinatal asphyxiatherapeutic hypothermia

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Area of Science:

  • Neonatal research
  • Immunology
  • Neuroscience

Background:

  • Neonatal encephalopathy (NE) is a serious condition with significant short- and long-term consequences.
  • Innate immune responses, involving cytokines like IL-8 and GM-CSF, are implicated in NE pathogenesis.
  • Predictive biomarkers for NE severity and neurodevelopmental outcomes are crucial.

Purpose of the Study:

  • To examine the association between innate immune cell activation markers (IL-8 and GM-CSF) and brain injury and outcomes in NE.
  • To compare these cytokine levels in NE infants with healthy neonatal controls.

Main Methods:

  • Serum and cerebrospinal fluid (CSF) samples were collected from term newborns with NE and controls on days 1, 3, and 7.
  • Duplex immunoassays were used to measure Interleukin-8 (IL-8) and Granulocyte-Macrophage-Colony-Stimulating-Factor (GM-CSF).
  • Biomarker levels were correlated with NE grade, seizures, MRI findings, mortality, and Bayley-III scores at 2 years.

Main Results:

  • Elevated day 2 serum IL-8 was associated with NE Grade II/III and predicted mortality.
  • GM-CSF levels varied, with decreased day 2 GM-CSF linked to abnormal MRI findings.
  • Elevated GM-CSF at 6-7 days of life negatively correlated with cognitive, language, and motor scores on the Bayley-III at 2 years.

Conclusions:

  • Moderate to severe NE and mortality are associated with elevated IL-8 levels.
  • GM-CSF may serve as a predictive biomarker for MRI abnormalities and neurodevelopmental outcomes (Bayley-III) in NE.
  • These findings highlight the role of inflammatory processes in NE and suggest potential for cytokine-based outcome prediction.