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The Journal of Neuroscience, July 1, 2001, 21(13):4649-4656
MIP-1 , MCP-1, GM-CSF, and TNF- Control the Immune Cell
Response That Mediates Rapid Phagocytosis of Myelin from the Adult
Mouse Spinal Cord
Shalina S.
Ousman and
Samuel
David
Centre for Research in Neuroscience, Montreal General Hospital
Research Institute and McGill University, Montréal, Québec,
Canada, H3G 1A4
The slow immune response in the adult mammalian CNS results
in slow myelin phagocytosis along degenerating white matter after injury. This has important consequences for axon regeneration because
of the presence of axon growth inhibitors in myelin. In addition,
abnormal immune cell responses in the CNS lead to demyelinating disease. Lysophosphatidylcholine (LPC) can induce an inflammatory response in the CNS, producing rapid demyelination without much damage
to adjacent cells. In this study, we searched for the molecular switches that turn on this immune cell response. Using reverse transcription PCR analysis, we show that mRNA expression of macrophage inflammatory protein-1 (MIP-1), macrophage chemotactic protein-1 (MCP-1), granulocyte macrophage-colony stimulating factor (GM-CSF), and
tumor necrosis factor- (TNF-) in the spinal cord is
rapidly and transiently upregulated after intraspinal injection of LPC. Neutralizing these signaling molecules with function-blocking antibodies suppresses recruitment of T-cells, neutrophils, and monocytes into the spinal cord, as well as significantly reduces the
number of phagocytic macrophages and the demyelination induced by LPC.
These findings will have important implications for CNS regeneration
and demyelinating disease.
Key words:
lysophosphatidylcholine; myelin; cytokine; chemokine; macrophage; T-cells
Copyright © 2001 Society for Neuroscience 0270-6474/01/21134649-08$05.00/0
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