S100B in the cerebrospinal fluid-A marker for glial damage in the rabbit model of pneumococcal meningitis

2010 | journal article. A publication with affiliation to the University of Göttingen.

Jump to: Cite & Linked | Documents & Media | Details | Version history

Cite this publication

​S100B in the cerebrospinal fluid-A marker for glial damage in the rabbit model of pneumococcal meningitis​
Schmidt, H.; Gerber, J.; Stuertz, K.; Djukic, M. ; Bunkowski, S.; Fischer, F. R. & Otto, M. et al.​ (2010) 
Neuroscience Letters475(2) pp. 104​-107​.​ DOI: https://doi.org/10.1016/j.neulet.2010.03.059 

Documents & Media


GRO License GRO License


Schmidt, H.; Gerber, Joachim; Stuertz, K.; Djukic, M. ; Bunkowski, Stephanie; Fischer, F. R.; Otto, Markus; Nau, R.
The rabbit model provides an important experimental setting for the evaluation of antibiotic agents against pneumococcal meningitis. One of the primary targets of this model is the study of neuronal and glial cell damage in bacterial meningitis. The aim of this investigation was to evaluate whether a significant increase of S100B in the cerebrospinal fluid (CSF) as an indicator of white matter damage could be observed in this meningitis model. Seven rabbits were infected intracisternally with S. pneumoniae, and CSF S100B concentrations were examined serially before infection, at 12h, 14h, 17h, 20h, and at 24h after infection. The course of CSF S100B increase and its relation to other parameters of brain tissue destruction and CSF inflammation were measured. Axonal damage was visualized by amyloid precursor protein (APP) immunostaining and demyelination by Luxol Fast Blue/Periodic Acid Schiff (LFB-PAS) stain. In each animal, we observed a distinct rise in S100B concentration in the CSF due to pneumococcal meningitis. We conclude that the CSF concentration of the glial S100B protein can be used as an additional parameter for future interventional studies focusing on glial cell damage in the rabbit model of bacterial meningitis. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
Issue Date
Elsevier Ireland Ltd
Neuroscience Letters 



Social Media