Excess glutamate in the cerebrospinal fluid in bacterial meningitis

• Verfasst von: Spranger, Matthias [VerfasserIn]
• Verfasst von: Krempien, Sebastian [VerfasserIn]
• Verfasst von: Schwab, Stefan [VerfasserIn]
• Verfasst von: Maiwald, Matthias [VerfasserIn]
• Verfasst von: Bruno, Kathleen [VerfasserIn]
• Verfasst von: Hacke, Werner [VerfasserIn]
• Titel: Excess glutamate in the cerebrospinal fluid in bacterial meningitis
• Verf.angabe: Matthias Spranger, Sebastian Krempien, Stefan Schwab, Matthias Maiwald, Kathleen Bruno, Werner Hacke
• E-Jahr: 1996
• Jahr: November 1996
• Umfang: 6 S.
• Fussnoten: Elektronische Reproduktion der Druck-Ausgabe 15. März 2000 ; Gesehen am 04.06.2025
• Titel Quelle: Enthalten in: Journal of the neurological sciences
• Ort Quelle: Amsterdam [u.a.] : Elsevier Science, 1964
• Jahr Quelle: 1996
• Band/Heft Quelle: 143(1996), 1, Seite 126-131
• ISSN Quelle: 1878-5883
• DOI: doi:10.1016/S0022-510X(96)00197-9
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Excitotoxicity
• Sach-SW: Glutamate
• Sach-SW: Macrophage
• Sach-SW: Meningitis
• K10plus-PPN: 1927439426

Abstract

We investigated possible neurotoxic components in the cerebrospinal fluid (CSF) of patients with bacterial meningitis. On murine cerebellar neuronal cell cultures, CSF exerted a dose-dependent toxic effect, which was attenuated by the NMDA receptor antagonist MK-801. Glutamate concentrations in the CSF of patients with bacterial meningitis were measured by an enzymatic assay and found to be significantly elevated (p < 0.001) as compared to viral meningitis and non-inflammatory neurological diseases. The concentration of glutamate in the CSF of patients with bacterial meningitis varied considerably and correlated with the severity of the disease as scored by the Glasgow Coma Scale. Cells in the CSF, mainly comprising polymorphonuclear granulocytes, did not release any glutamate into the culture medium, whereas blood monocytes produced remarkable amounts. These findings implicate an important role of monocytic inflammatory cells in bacterial meningitis by the release of glutamate, which may contribute to neuronal cell death.