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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Neurosci
2017 ; 37
(43
): 10258-10277
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Neutrophils Are Critical for Myelin Removal in a Peripheral Nerve Injury Model of
Wallerian Degeneration
#MMPMID28912156
Lindborg JA
; Mack M
; Zigmond RE
J Neurosci
2017[Oct]; 37
(43
): 10258-10277
PMID28912156
show ga
Wallerian degeneration (WD) is considered an essential preparatory stage to the
process of axonal regeneration. In the peripheral nervous system, infiltrating
monocyte-derived macrophages, which use the chemokine receptor CCR2 to gain entry
to injured tissues from the bloodstream, are purportedly necessary for efficient
WD. However, our laboratory has previously reported that myelin clearance in the
injured sciatic nerve proceeds unhindered in the Ccr2(-/-) mouse model. Here, we
extensively characterize WD in male Ccr2(-/-) mice and identify a compensatory
mechanism of WD that is facilitated primarily by neutrophils. In response to the
loss of CCR2, injured Ccr2(-/-) sciatic nerves demonstrate prolonged expression
of neutrophil chemokines, a concomitant extended increase in the accumulation of
neutrophils in the nerve, and elevated phagocytosis by neutrophils. Neutrophil
depletion substantially inhibits myelin clearance after nerve injury in both male
WT and Ccr2(-/-) mice, highlighting a novel role for these cells in peripheral
nerve degeneration that spans genotypes.SIGNIFICANCE STATEMENT The accepted view
in the basic and clinical neurosciences is that the clearance of axonal and
myelin debris after a nerve injury is directed primarily by inflammatory CCR2(+)
macrophages. However, we demonstrate that this clearance is nearly identical in
WT and Ccr2(-/-) mice, and that neutrophils replace CCR2(+) macrophages as the
primary phagocytic cell. We find that neutrophils play a major role in myelin
clearance not only in Ccr2(-/-) mice but also in WT mice, highlighting their
necessity during nerve degeneration in the peripheral nervous system. These
degeneration studies may propel improvements in nerve regeneration and draw
critical parallels to mechanisms of nerve degeneration and regeneration in the
CNS and in the context of peripheral neuropathies.
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