S100B modulates IL-6 release and cytotoxicity from hypothermic brain cells and inhibits hypothermia-induced axonal outgrowth

Brain protection is essential during neonatal and pediatric cardiac surgery. Deep hypothermia is still the most important method for achieving neuroprotection during cardiopulmonary bypass. Previously, we could demonstrate that deep hypothermia induces substantial cytotoxicity in brain cells as well...

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Bibliographic Details
Published in:Neuroscience research 2007-09, Vol.59 (1), p.68-73
Main Authors: Schmitt, Katharina R.L., Kern, Claudia, Lange, Peter E., Berger, Felix, Abdul-Khaliq, Hashim, Hendrix, Sven
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Astrocytes
Astrocytes - drug effects
Axons - drug effects
Axons - physiology
Brain - cytology
BV-2 microglial cells
Cell Survival - drug effects
Cell Survival - physiology
Cells, Cultured
Hypothermia
IL-6
Interleukin-6 - metabolism
Mice
Nerve Growth Factors - pharmacology
Neurons
Neurons - cytology
Neurons - drug effects
Neurons - metabolism
Neuroregeneration
Organ Culture Techniques
Organotypic brain slice
S100 Calcium Binding Protein beta Subunit
S100 Proteins - pharmacology
Statistics, Nonparametric
Temperature
Time Factors
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Summary:Brain protection is essential during neonatal and pediatric cardiac surgery. Deep hypothermia is still the most important method for achieving neuroprotection during cardiopulmonary bypass. Previously, we could demonstrate that deep hypothermia induces substantial cytotoxicity in brain cells as well as increased release of the pro-inflammatory cytokine interleukin-6 (IL-6), which plays an important role in neuroprotection and neuroregeneration. Deep hypothermia is also associated with increased levels of the astrocytic protein S100B in the serum and cerebrospinal fluid of patients. Since S100B may modulate pro-inflammatory cytokines and may stimulate neurite outgrowth, we have tested the hypothesis that nanomolar concentrations of S100B may increase IL-6 release from brain cells and support axonal outgrowth from organotypic brain slices under hypothermic conditions. S100B administration substantially reduced neuronal and glial cytotoxicity under hypothermic conditions. In the presence of S100B hypothermia-induced IL-6 release in primary astrocytes was significantly increased but reduced in BV-2 microglial cells and primary neurons. Surprisingly, deep hypothermia increased axonal outgrowth from brain slices and – in contrast to our hypothesis – this hypothermia-induced neurite outgrowth was inhibited by S100B. These data suggest that S100B differentially influences cytokine release and cytotoxicity from distinct brain cells and may inhibit neuroregeneration by suppressing hypothermia-induced axonal outgrowth.
ISSN:0168-0102
1872-8111
DOI:10.1016/j.neures.2007.05.011