Interleukin-1beta potentiates neuronal injury in a variety of injury models involving energy deprivation.
The purpose of this study was to develop a suitable in vitro model system to study the biochemical pathway(s) by which interleukin-1beta (IL-1beta) contributes to the pathogenesis of cerebral ischemia. Thus, the effect of IL-1beta on a number of injury paradigms associated with energy deprivation was investigated using murine mixed cortical cell cultures. While IL-1beta by itself was not neurotoxic, pre-treatment-but not concurrent or post-treatment-with this cytokine potentiated neuronal injury induced by depriving cultures of either oxygen, glucose, or both oxygen and glucose. Cytotoxicity was abolished by an IL-1beta-neutralizing antibody. Together, these results demonstrate the establishment of reliable and reproducible in vitro models that will now allow detailed investigation of the cellular and molecular mechanisms relating to IL-1beta-mediated neuronal cell death.
Fogal
Birgit
B
University of Connecticut Health Center; Department of Neuroscience, MC-3401, Farmington, CT 06030-3401, USA.
Hewett
James A
JA
Hewett
Sandra J
SJ
D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D002545:Brain Ischemia / Q000503:physiopathology*; D002452:Cell Count / Q000379:methods; D016923:Cell Death / Q000187:drug effects; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005947:Glucose / Q000172:deficiency*; D007003:Hypoglycemia / Q000503:physiopathology; D000860:Hypoxia; D007375:Interleukin-1 / Q000008:administration & dosage / Q000009:adverse effects*; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D011419:Propidium; D051381:Rats; D013997:Time Factors
D007375:Interleukin-1; D011419:Propidium; D005947:Glucose