Chemokine-Ligands/Receptors: Multiplayers in Traumatic Spinal Cord Injury

Figure 2

Chemokine-ligand/receptor-expression after impact SCI in adult rats. After impact lesions, different chemokines are induced in distinct anatomical regions along the whole neuraxis. This overview exemplarily illustrates chemokine-ligand/receptor-immunostaining along the neuraxis (diaminobenzidine and double/triple-immunofluorescence labeling). Schemes indicate anatomical location. On brain level, CCL2/CCR2 expression was found induced in thalamic nuclei in the late time-course, that is, 42 hours after severe SCI, which was colocalized with TRPV1 and CB1. Sham animals did not exhibit chemokine expression in this location. On lesion level T9 chemokine-ligands/receptors were induced in inflammatory cells in the early and astroglial cells in the later time-course. Furthermore, chemokines were induced in the ventrolateral white matter along the whole spinal cord. Here, chemokines colocalized with proliferating BrdU-labeled cells, which coexpressed astroglia and NPC markers (shown for nestin). In vitro, CCR1 was found consistently expressed on endogenous NPCs (demonstrated for a sham-derived neurosphere). Applying CCL3 to NPCs during differentiation cycles led to significant higher GFAP-mRNA and immunohistochemical level as compared to untreated neurosphere cultures (demonstrated for sham-derived cultures). Another anatomical location of chemokine induction was pain-related spinal cord areas like dorsal horns and dorsal columns. Here, chemokine expression colocalized among others with TRPV1 and glial markers. Details are discussed in the respective sections.