Impact of indolent inflammation on neonatal hypoxic‐ischemic brain injury in mice

This report describes a new experimental model to evaluate the effect of a recurrent systemic inflammatory challenge, after cerebral hypoxia‐ischemia in immature mice, on the progression of brain injury. Treatment with a low dose of lipopolysaccharide (E. coli O55:B5, 0.2 mg/kg for 3 days, then 0.1...

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Bibliographic Details
Published in:International journal of developmental neuroscience 2008-02, Vol.26 (1), p.57-65
Main Authors: Barks, John D.E., Liu, Yi‐Qing, Shangguan, Yu, Li, Joyce, Pfau, Jennifer, Silverstein, Faye S.
Format: Article
Language:English
Subjects:
Age Factors
Analysis of Variance
Animals
Animals, Newborn
Blood Glucose - drug effects
Body Temperature - drug effects
Body Temperature - physiology
Brain Injuries - etiology
Brain Injuries - pathology
Bromodeoxyuridine - metabolism
Cell Proliferation - drug effects
Cerebral ischemia
Disease Models, Animal
Escherichia coli
Functional Laterality
Hypoxia-Ischemia, Brain - complications
Hypoxia‐ischemia
Inflammation
Inflammation - chemically induced
Lateral Ventricles - pathology
Lipopolysaccharide
Lipopolysaccharides - administration & dosage
Mice
Myelination
Neonatal
Neurogenesis
Perinatal
Prosencephalon - pathology
Subventricular zone
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Summary:This report describes a new experimental model to evaluate the effect of a recurrent systemic inflammatory challenge, after cerebral hypoxia‐ischemia in immature mice, on the progression of brain injury. Treatment with a low dose of lipopolysaccharide (E. coli O55:B5, 0.2 mg/kg for 3 days, then 0.1 mg/kg for 2 days) daily for 5 days after unilateral cerebral hypoxia‐ischemia (right carotid ligation followed by 35 min in 10% O2) in 10‐day‐old mice resulted in increased right forebrain tissue damage (35.6% reduction in right hemisphere volume compared to 20.6% reduction in saline‐injected controls), in bilateral reductions in corpus callosum area (by 12%) and myelin basic protein immunostaining (by 19%), and in suppression of injury‐related right subventricular zone cellular proliferation. The post‐hypoxic‐ischemic lipopolysaccharide regimen that amplified brain injury was not associated with increased mortality, nor with changes in body temperature, weight gain or blood glucose concentrations. The results of the present study demonstrate that systemic inflammation influences the evolution of tissue injury after neonatal cerebral hypoxia‐ischemia and may also impair potential recovery mechanisms.
ISSN:0736-5748
1873-474X
DOI:10.1016/j.ijdevneu.2007.08.005