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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+Neuroinflammation
2018 ; 15
(1
): 192
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Molecular and cellular identification of the immune response in peripheral
ganglia following nerve injury
#MMPMID29945607
Lindborg JA
; Niemi JP
; Howarth MA
; Liu KW
; Moore CZ
; Mahajan D
; Zigmond RE
J Neuroinflammation
2018[Jun]; 15
(1
): 192
PMID29945607
show ga
BACKGROUND: Neuroinflammation accompanies neural trauma and most neurological
diseases. Axotomy in the peripheral nervous system (PNS) leads to dramatic
changes in the injured neuron: the cell body expresses a distinct set of genes
known as regeneration-associated genes, the distal axonal segment degenerates and
its debris is cleared, and the axons in the proximal segment form growth cones
and extend neurites. These processes are orchestrated in part by immune and other
non-neuronal cells. Macrophages in ganglia play an integral role in supporting
regeneration. Here, we explore further the molecular and cellular components of
the injury-induced immune response within peripheral ganglia. METHODS: Adult male
wild-type (WT) and Ccr2 (-/-) mice were subjected to a unilateral transection of
the sciatic nerve and axotomy of the superior cervical ganglion (SCG). Antibody
arrays were used to determine the expression of chemokines and cytokines in the
dorsal root ganglion (DRG) and SCG. Flow cytometry and immunohistochemistry were
utilized to identify the cellular composition of the injury-induced immune
response within ganglia. RESULTS: Chemokine expression in the ganglia differed
48 h after nerve injury with a large increase in macrophage inflammatory
protein-1? in the SCG but not in the DRG, while C-C class chemokine ligand 2 was
highly expressed in both ganglia. Differences between WT and Ccr2 (-/-) mice were
also observed with increased C-C class chemokine ligand 6/C10 expression in the
WT DRG compared to C-C class chemokine receptor 2 (CCR2)(-/-) DRG and increased
CXCL5 expression in CCR2(-/-) SCG compared to WT. Diminished macrophage
accumulation in the DRG and SCG of Ccr2 (-/-) mice was found compared to WT
ganglia 7 days after nerve injury. Interestingly, neutrophils were found in the
SCG but not in the DRG. Cytokine expression, measured 7 days after injury,
differed between ganglion type and genotype. Macrophage activation was assayed by
colabeling ganglia with the anti-inflammatory marker CD206 and the macrophage
marker CD68, and an almost complete colocalization of the two markers was found
in both ganglia. CONCLUSIONS: This study demonstrates both molecular and cellular
differences in the nerve injury-induced immune response between DRG and SCG and
between WT and Ccr2 (-/-) mice.