Related Experiment Video

Updated: Aug 8, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

Interleukin-8 released into the cerebrospinal fluid after brain injury is associated with blood-brain barrier

T Kossmann1, P F Stahel, P M Lenzlinger

  • 1Division of Trauma Surgery, University of Zürich Medical School, Switzerland.

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|March 1, 1997
PubMed

Insights

Interleukin-8 (IL-8) is elevated in cerebrospinal fluid after severe traumatic brain injury, suggesting it drives nerve growth factor (NGF) production and contributes to brain injury pathology.

Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Severe traumatic brain injury (TBI) can lead to complex inflammatory responses within the central nervous system.
  • The role of specific cytokines, such as Interleukin-8 (IL-8), in TBI pathogenesis requires further elucidation.
  • Understanding the interplay between inflammatory mediators and neurotrophic factors is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the levels and potential role of Interleukin-8 (IL-8) in the cerebrospinal fluid (CSF) of patients with severe traumatic brain injury (TBI).
  • To explore the relationship between IL-8, blood-brain barrier (BBB) integrity, and the presence of Nerve Growth Factor (NGF) in TBI patients.
  • To determine if IL-8 directly influences NGF production in astrocytes and assess the efficacy of anti-IL-8 antibodies in mitigating this effect.

Main Methods:

  • Measurement of IL-8 levels in CSF and serum from 14 severe TBI patients.
  • Assessment of blood-brain barrier (BBB) dysfunction based on IL-8 CSF levels.
  • Detection of Nerve Growth Factor (NGF) in CSF and correlation with IL-8 concentrations.
  • In vitro experiments using cultured astrocytes exposed to CSF with varying IL-8 levels to measure NGF production.
  • Application of anti-IL-8 antibodies to assess their impact on NGF release.

Main Results:

  • IL-8 levels were significantly higher in CSF compared to serum in TBI patients, indicating intrathecal production.
  • Elevated CSF IL-8 levels correlated with severe blood-brain barrier dysfunction.
  • Patients with detectable NGF in CSF had significantly higher IL-8 concentrations.
  • CSF containing high IL-8 concentrations stimulated greater NGF production in cultured astrocytes compared to low IL-8 samples.
  • Anti-IL-8 antibodies partially inhibited NGF release, with complete inhibition not achieved, suggesting the involvement of other cytokines like TNF-alpha and IL-6.

Conclusions:

  • IL-8 is a key inflammatory mediator in the CSF following severe TBI, likely produced intrathecally.
  • IL-8 plays a significant role in inducing NGF production in astrocytes, potentially exacerbating TBI pathology.
  • The findings suggest IL-8 is a pivotal cytokine in brain injury and a potential therapeutic target, possibly in combination with other anti-inflammatory agents.

More Related Videos

Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury07:21

Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury

Published on: May 27, 2022

Stab-Wound Mouse Model for Studying Hemorrhage and Inflammation in Traumatic Brain Injury04:03

Stab-Wound Mouse Model for Studying Hemorrhage and Inflammation in Traumatic Brain Injury

Published on: February 21, 2025

Related Concept Videos

The Blood-brain Barrier00:49

The Blood-brain Barrier

Overview
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
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...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...