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Microglia expressing interleukin-13 undergo cell death and contribute to neuronal survival in vivo.

Authors
Shin, WH; Lee, DY; Park, KW; Kim, SU; Yang, MS; Joe, EH; Jin, BK
Citation
Glia, 46(2):142-152, 2004
Journal Title
Glia
ISSN
0894-14911098-1136
Abstract
How to minimize brain inflammation is pathophysiologically important, since inflammation induced by microglial activation can exacerbate brain damage. In the present report, we show that injection of lipopolysaccharide (LPS) into the rat cortex led to increased levels of interleukin-13 (IL-13) and to IL-13 immunoreactivity, followed by the substantial loss of microglia at 3 days post-LPS. IL-13 levels in LPS-injected cortex reached a peak at 12 h post-injection, remained elevated at 24 h, and returned to basal levels at day 4. In parallel, IL-13 immunoreactivity was detected as early as 12 h post-LPS and maintained up to 24 h; it disappeared at 4 days. Surprisingly, IL-13 immunoreactivity was detected exclusively in microglia, but not in neurons or astrocytes. Following treatment with LPS in vitro, IL-13 expression was also induced in microglia in the presence of neurons, but not in the presence of astrocytes or in cultured pure microglia alone. In experiments designed to determine the involvement of IL-13 in microglia cell death, IL-13-neutralizing antibodies significantly increased survival of activated microglia at 3 days post-LPS. Consistent with these results, the expression of inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-alpha) was sustained in activated microglia and neuronal cell death was consequently increased. Taken together, the present study is the first to demonstrate the endogenous expression of IL-13 in LPS-activated microglia in vivo, and to demonstrate that neurons may be required for IL-13 expression in microglia. Our data strongly suggest that IL-13 may control brain inflammation by inducing the death of activated microglia in vivo, resulting in an enhancement of neuronal survival.
MeSH terms
AnimalsAntibodies/pharmacologyApoptosis/drug effects/*physiologyCell Communication/physiologyCell Survival/physiologyCells, CulturedCerebral Cortex/cytologyFemaleGene ExpressionInterleukin-13/*genetics/immunologyLipopolysaccharides/pharmacologyMicroglia/*cytology/*physiologyNeurons/*cytologyNitric Oxide Synthase/geneticsNitric Oxide Synthase Type IIRatsRats, Sprague-DawleyTumor Necrosis Factor-alpha/genetics
DOI
10.1002/glia.10357
PMID
15042582
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
Journal Papers > Research Organization > Institute for Medical Sciences
AJOU Authors
김, 승업양, 명순조, 은혜진, 병관
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