Rifampin reduces production of reactive oxygen species of cerebrospinal fluid phagocytes and hippocampal neuronal apoptosis in experimental Streptococcus pneumoniae meningitis
2000 | journal article. A publication with affiliation to the University of Göttingen.
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Rifampin reduces production of reactive oxygen species of cerebrospinal fluid phagocytes and hippocampal neuronal apoptosis in experimental Streptococcus pneumoniae meningitis
Bottcher, T.; Gerber, J.; Wellmer, A.; Smirnov, A. V.; Fakhrjanali, F.; Mix, E. & Pilz, J. et al. (2000)
The Journal of Infectious Diseases, 181(6) pp. 2095-2098. DOI: https://doi.org/10.1086/315518
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Details
- Authors
- Bottcher, T.; Gerber, Joachim; Wellmer, A.; Smirnov, A. V.; Fakhrjanali, F.; Mix, E.; Pilz, J.; Zettl, Uwe K.; Nau, R.
- Abstract
- Bacterial compounds induce the production of reactive oxygen species (ROS) in meningitis. Rifampin releases smaller quantities of proinflammatory compounds from Streptococcus pneumoniae than do beta-lactam antibiotics. Therefore, rabbits infected intracisternally with S. pneumoniae were treated intravenously either with rifampin 5 mg/kg/h or ceftriaxone 10 mg/kg/h (n = 9 each). Before initiation of antibiotic treatment, a strong positive correlation between ROS production of cerebrospinal fluid (CSF) phagocyte populations and bacterial CSF titers was observed (granulocytes: r(s) = .90, P < .0001; monocytes: r(s) = .81, P < .0001). CSF leukocytes from rifampin-treated rabbits produced less ROS (monocytes at 2 h after initiation of treatment: P = .045; at 5 h: P = .014; granulocytes at 5 h: P = .036) than did leukocytes from animals receiving ceftriaxone. The CSF malondialdehyde concentrations and the density of apoptotic neurons in the dentate gyrus were lower in rifampin- than in ceftriaxone-treated animals (P = .002 and .005). The use of rifampin to reduce the release of ROS and to decrease secondary brain injury appears promising.
- Issue Date
- 2000
- Status
- published
- Publisher
- Univ Chicago Press
- Journal
- The Journal of Infectious Diseases
- ISSN
- 0022-1899