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Fas (APO-1/CD95) in inflammatory CNS diseases: intrathecal release in bacterial meningitis

K Fassbender1, C Eschenfelder, M Hennerici

  • 1Department of Neurology, Klinikum Mannheim, University of Heidelberg, Germany.

Journal of Neuroimmunology
|June 23, 1999
PubMed

Insights

Fas (APO-1, CD95) release increased in bacterial meningitis, suggesting granulocyte apoptosis in the subarachnoidal space limits inflammation. This finding was specific to bacterial meningitis, not viral meningoencephalitis or multiple sclerosis.

Area of Science:

  • Neuroimmunology
  • Cellular Biology
  • Infectious Diseases

Background:

  • Fas (APO-1, CD95) is a type L-membrane protein critical for cytokine-mediated apoptosis.
  • Apoptosis plays a role in regulating inflammatory responses in the central nervous system.

Purpose of the Study:

  • To investigate the intrathecal release of Fas in bacterial meningitis, viral meningoencephalitis, and multiple sclerosis in vivo.
  • To determine if Fas release is associated with specific neurological inflammatory conditions.

Main Methods:

  • In vivo investigation of Fas release in cerebrospinal fluid (CSF).
  • Correction for blood-brain-CSF barrier disruption.
  • Comparison of Fas levels across different neurological diseases.

Main Results:

  • Significantly increased intrathecal release of Fas was observed exclusively in bacterial meningitis.
  • No significant increase in Fas release was detected in viral meningoencephalitis or multiple sclerosis.
  • The elevated Fas release in bacterial meningitis suggests a role in granulocyte apoptosis.

Conclusions:

  • Intrathecal Fas release is a specific marker for bacterial meningitis.
  • Granulocyte apoptosis in the subarachnoidal space may serve to self-limit the inflammatory host response in bacterial meningitis.
  • Fas-mediated apoptosis may not be a primary mechanism in the studied viral or demyelinating diseases.

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