Involvement of monocyte chemoattractant protein-1, macrophage inflammatory protein-1α and interleukin-1β in Wallerian degeneration (original) (raw)

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Centre for Research in Neuroscience, McGill University Health Center, Montreal, Quebec, Canada

Correspondence to: Dr Samuel David, Centre for Research in Neuroscience, Montreal General Hospital Research Institute, Livingston Hall, Room L7-210, 1650 Cedar Ave, Montreal, Quebec, Canada, H3G 1A4 E-mail: sam.david@mcgill.ca

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Centre for Research in Neuroscience, McGill University Health Center, Montreal, Quebec, Canada

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Marcelino Avilés-Trigueros

Centre for Research in Neuroscience, McGill University Health Center, Montreal, Quebec, Canada

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Centre for Research in Neuroscience, McGill University Health Center, Montreal, Quebec, Canada

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Received:

13 September 2004

Revision received:

19 December 2004

Accepted:

22 December 2004

Published:

02 February 2005

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Florence E. Perrin, Steve Lacroix, Marcelino Avilés-Trigueros, Samuel David, Involvement of monocyte chemoattractant protein-1, macrophage inflammatory protein-1α and interleukin-1β in Wallerian degeneration, Brain, Volume 128, Issue 4, April 2005, Pages 854–866, https://doi.org/10.1093/brain/awh407
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Abstract

Wallerian degeneration in the CNS and PNS consists of degradation and phagocytosis of axons and their myelin sheath distal to the site of injury. This process of degeneration, which requires an effective macrophage response, occurs rapidly in peripheral nerves but is slow in the CNS. Rapid Wallerian degeneration in peripheral nerves may contribute to subsequent axonal regeneration. We show that there is a marked increase in mRNA expression of three pro-inflammatory molecules, the chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α), and the cytokine interleukin-1β (IL-1β), in the mouse sciatic nerve but not in the spinal cord undergoing Wallerian degeneration. Neutralizing MCP-1, MIP-1α and IL-1β in the lesioned sciatic nerve with function-blocking antibodies suppressed macrophage responses and myelin clearance. Injecting recombinant MCP-1, MIP-1α or IL-1β into the normal, uninjured spinal cord triggered the expression of a number of chemokines and cytokines. Furthermore, injecting recombinant MCP-1/MIP-1α or IL-1β into the dorsal column of the spinal cord undergoing Wallerian degeneration triggered rapid macrophage/microglial activation and myelin clearance. These findings provide direct evidence that MCP-1, MIP-1α and IL-1β are important regulators of macrophage responses that lead to rapid myelin breakdown and clearance in Wallerian degeneration.

GM-CSF = granulocyte–macrophage colony-stimulating factor, IFN-γ = interferon-γ, IL-1β = interleukin-1β, IL-10 = interleukin-10, MCP-1 = monocyte chemoattractant protein-1, MIP-1α = macrophage inflammatory protein-1α, RANTES = regulated upon activation, normal T cell expressed and secreted, RPA = RNase protection assay, TGF-β1 = transforming growth factor-β1, TNF-α = tumour necrosis factor-α

© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Topic:

• cytokine
• chemokines
• interleukins
• macrophages
• monocyte chemoattractant protein-1
• rna, messenger
• sciatic nerve
• wallerian degeneration
• antibodies
• mice
• spinal cord
• myelin

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