| Literature DB >> 16732273 |
Astrid E Cardona1, Erik P Pioro, Margaret E Sasse, Volodymyr Kostenko, Sandra M Cardona, Ineke M Dijkstra, Deren Huang, Grahame Kidd, Stephen Dombrowski, RanJan Dutta, Jar-Chi Lee, Donald N Cook, Steffen Jung, Sergio A Lira, Dan R Littman, Richard M Ransohoff.
Abstract
Microglia, the resident inflammatory cells of the CNS, are the only CNS cells that express the fractalkine receptor (CX3CR1). Using three different in vivo models, we show that CX3CR1 deficiency dysregulates microglial responses, resulting in neurotoxicity. Following peripheral lipopolysaccharide injections, Cx3cr1-/- mice showed cell-autonomous microglial neurotoxicity. In a toxic model of Parkinson disease and a transgenic model of amyotrophic lateral sclerosis, Cx3cr1-/- mice showed more extensive neuronal cell loss than Cx3cr1+ littermate controls. Augmenting CX3CR1 signaling may protect against microglial neurotoxicity, whereas CNS penetration by pharmaceutical CX3CR1 antagonists could increase neuronal vulnerability.Entities:
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Year: 2006 PMID： 16732273 DOI： 10.1038/nn1715
Source DB: PubMed Journal: Nat Neurosci ISSN： 1097-6256 Impact factor: 24.884