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Increased cerebrospinal fluid concentrations of soluble Fas (CD95/Apo-1) in hydrocephalus

U Felderhoff-Mueser1, R Herold, F Hochhaus

  • 1Department of Neonatology, Charité Children's Hospital, Virchow Klinikum, Humboldt University, Augustenburger Platz 1, 13353 Berlin, Germany. ursula.felderhoff@charite.de

Archives of Disease in Childhood
|March 22, 2001
PubMed

Insights

Children with hydrocephalus have high levels of soluble Fas (sFas) in their cerebrospinal fluid (CSF). This suggests the body may be producing sFas to counteract pressure-induced brain cell death.

Area of Science:

  • Pediatric Neurology
  • Neuroscience
  • Cell Biology

Background:

  • Chronically elevated intracranial pressure (ICP) in children leads to ventricular enlargement and secondary brain tissue loss.
  • Apoptosis (programmed cell death) is a key mechanism of neuronal injury in hydrocephalus models.
  • Fas/Fas ligand interactions regulate apoptotic cell death pathways.

Purpose of the Study:

  • To investigate the role of apoptosis-regulating cytokines in pediatric hydrocephalus.
  • To measure levels of soluble Fas (sFas) and soluble Fas ligand (sFasL) in cerebrospinal fluid (CSF) of children with hydrocephalus.

Main Methods:

  • CSF samples were collected from 31 children with symptomatic hydrocephalus undergoing shunt surgery.
  • CSF samples from 18 healthy children served as controls.
  • Concentrations of sFas and sFasL were quantified using immunoassays.

Main Results:

  • Significantly elevated concentrations of sFas were detected in the CSF of children with hydrocephalus (median 252 ng/ml).
  • sFas levels in control subjects were below the detection limit (<0.5 ng/ml).
  • sFasL was undetectable in nearly all samples.

Conclusions:

  • Elevated CSF sFas in hydrocephalic children indicates intrinsic production of sFas.
  • This intrinsic sFas production may serve a protective role by antagonizing Fas-mediated apoptosis induced by pressure.
  • Findings suggest a potential therapeutic target for managing brain injury in pediatric hydrocephalus.
Abstract

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