Inflammatory mediators and neonatal brain damage

Citation
E. Saliba et A. Henrot, Inflammatory mediators and neonatal brain damage, BIOL NEONAT, 79(3-4), 2001, pp. 224-227
Citations number
44
Categorie Soggetti
Medical Research General Topics
Journal title
BIOLOGY OF THE NEONATE
ISSN journal
00063126 → ACNP
Volume
79
Issue
3-4
Year of publication
2001
Pages
224 - 227
Database
ISI
SICI code
0006-3126(2001)79:3-4<224:IMANBD>2.0.ZU;2-K
Abstract
Inflammatory mediators are multifunctional cytokines that play important ro les both in normal central nervous system (CNS) development and in the resp onse of the brain to diverse forms of injury. Interleukin (IL)-1 beta, tumo r necrosis factor-alpha and IL-6 are among the best-characterized early-res ponse cytokines. Recent data suggest that they may be synthesized and secre ted by several CNS cell types, including microglia, astrocytes and neurons. Biological effects of these cytokines that could influence the progression of injury in the brain include stimulating the synthesis of other cytokine s and neuronal injury mediators such as nitric oxide synthase, inducing leu kocyte infiltration and the expression of adhesion molecules, influencing g lial gene expression and damaging oligodendrocytes. In the immature brain, proinflammatory cytokines might lead to white matter damage during prenatal intrauterine infection and contribute to progressive neuronal damage in ac ute brain injury evoked by cerebral hypoxia-ischemia. Interrupting the proi nflammatory cascade might limit the extent of irreversible injury. Copyrigh t (C) 2001 S. Karger AG. Basel.