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Inflammatory response during bacterial meningitis is unchanged in Fas- and Fas ligand-deficient mice

Robert Paul1, Barbara Angele, Bernd Sporer

  • 1Department of Neurology, Klinikum Grosshadern, Ludwig-Maximilians-University of Munich, Marchioninistr. 15, 81377 Munich, Germany.

Journal of Neuroimmunology
|June 30, 2004
PubMed

Insights

Fas and Fas ligand (FasL) are not essential in bacterial meningitis. Studies show these molecules do not significantly alter the inflammatory response or disease severity in mice with pneumococcal meningitis.

Area of Science:

  • Neuroscience
  • Immunology
  • Infectious Diseases

Background:

  • Fas (CD95) and Fas ligand (FasL, CD95L) are implicated in acute inflammation and neutrophil regulation.
  • Elevated soluble Fas and FasL levels are observed in cerebrospinal fluid (CSF) of bacterial meningitis patients.

Purpose of the Study:

  • To investigate the role of Fas and FasL in the pathophysiology of pneumococcal meningitis using knockout mouse models.

Main Methods:

  • Utilized functional FasL (gld) and Fas (lpr)-deficient mice.
  • Induced pneumococcal meningitis in wild-type (WT) and knockout mice.
  • Monitored CSF white blood cell (WBC) count, intracranial pressure (ICP), and vessel permeability.
  • Assessed clinical status and measured inflammatory markers (IL-1beta, MMP-2, MMP-9) in the brain.

Main Results:

  • Pneumococcal meningitis induction in WT mice led to increased CSF WBC, ICP, vessel permeability, and worsened clinical status.
  • Inflammatory response in WT mice included elevated IL-1beta, MMP-2, and MMP-9.
  • No significant differences in pathophysiological alterations were observed between gld/lpr-deficient mice and WT mice.

Conclusions:

  • Fas and FasL are not essential for regulating the acute inflammatory response during pneumococcal meningitis.
  • The Fas/FasL pathway does not play a critical role in the studied aspects of pneumococcal meningitis pathophysiology.

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