| Accession Number | <strong>00004647-200412000-00003</strong>. |
|---|---|
| Author | Hedtjarn, Maj *; Mallard, Carina *; Hagberg, Henrik *+ |
| Institution | Departments of *Physiology and Pharmacology and +Obstetrics and Gynecology, Perinatal Center, Goteborg, University, Goteborg, Sweden |
| Title | |
| Source | Journal of Cerebral Blood Flow & Metabolism. 24(12):1333-1351, December 2004. |
| Abstract | Summary: Brain ischemia triggers an inflammatory reaction that progresses for days to weeks and seems to have a role in secondary progression of injury. Inflammation induces a complex pattern of signaling molecules with partly contradictory actions, and the responses may be different in the immature and adult brain. The authors characterized the global inflammatory gene expression in the developing brain as a first step toward understanding the protective and deleterious effects of inflammation after hypoxia-ischemia. Oligonucleotide arrays were used to investigate inflammatory genes in cortex, hippocampus, thalamus, and striatum at 2, 8, 24, and 72 hours after hypoxia-ischemia, which was induced in 9-day-old mice by left carotid artery ligation followed by hypoxia. After hypoxia-ischemia, 148 inflammatory genes were differentially expressed. More than 97% of the genes were upregulated and 93% had not previously been reported after hypoxia-ischemia in the immature brain. The results indicate that microglia/macrophages, T- and B-cells, NK-cells, mast cells, dendritic cells, and polymorphonuclear leukocytes may participate in the response to hypoxia-ischemia. In addition, novel cytokines/chemokines, complement-related, interferon-regulated, components of the TIR/nuclear factor-[kappa]B pathway, and a number of immunomodulatory genes were induced. Several of these genes may of pathophysiologic significance after neonatal hypoxia-ischemia. Copyright (C) 2004 International Society of Cerebral Blood Flow and Metabolism |