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Evaluation of Host-Pathogen Responses and Vaccine Efficacy in Mice
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TRAIL limits excessive host immune responses in bacterial meningitis
Olaf Hoffmann1, Josef Priller, Timour Prozorovski
1Department of Neurology, Laboratory of Molecular Psychiatry, Charité Universitätsmedizin Berlin, Berlin, Germany.
The Journal of Clinical Investigation
|June 16, 2007
Summary
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) reduces inflammation and neuronal cell death in experimental meningitis. This suggests TRAIL could be a novel anti-inflammatory agent for invasive infections.
Area of Science:
- Immunology
- Neuroscience
- Molecular Biology
Background:
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) plays a role in immune responses.
- Its anti-inflammatory effects in central nervous system (CNS) infections are not well understood.
Purpose of the Study:
- To investigate the anti-inflammatory effects of TRAIL in experimental meningitis.
- To explore TRAIL's potential as a therapeutic agent for CNS inflammation.
Main Methods:
- Used TRAIL-deficient (TRAIL-/-) mice and wild-type mice with experimentally induced meningitis.
- Administered recombinant TRAIL (rTRAIL) intrathecally and via bone marrow reconstitution.
- Analyzed inflammation, clinical impairment, apoptosis in the hippocampus, and intrathecal TRAIL synthesis in patients.
Main Results:
- TRAIL-/- mice exhibited prolonged inflammation, increased clinical impairment, and hippocampal apoptosis.
- rTRAIL administration or wild-type bone marrow reconstitution reversed these detrimental effects.
- Intrathecal rTRAIL reduced inflammation and apoptosis in wild-type mice with meningitis.
- Bacterial meningitis patients showed increased intrathecal TRAIL synthesis.
Conclusions:
- TRAIL acts as a negative regulator of acute CNS inflammation.
- TRAIL can reduce inflammation and neuronal cell death in meningitis.
- TRAIL holds potential as a novel anti-inflammatory therapeutic for invasive infections.
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