Figure 2.

CXCR2 promotes spontaneous recovery and oligodendrocyte survival during chronic JHMV infection. C57BL/6 mice were infected with JHMV and their spinal cords removed at the indicated time points. (A) mRNA for CXCR2, CXCL1, and CXCL2 are upregulated within the spinal cords of JHMV infected mice. (B) Immunofluorescence staining reveals that the majority of CXCL1 (green) co-localizes with GFAP-positive (red) astrocytes within the spinal cord white matter. (C) Neutralization of CXCR2 (from day 12–20 pi) delays clinical recovery from chronic JHMV infection. (D and E) Mice receiving CXCR2 antiserum had significantly greater total areas of demyelination within the spinal cord. Representative luxol fast blue stained spinal cords are shown in panel (D) with the total (solid line) and demyelinated (dashed line) white matter indicated. (F) Significantly (p < 0.001) increased numbers of apoptotic (TUNEL+) cells were observed within the spinal cords of anti-CXCR2 treated mice. (G) CXCL1, in a dose-dependent manner, protects oligodendrocytes from apoptosis, and (H) CXCR2-deficienct oligodendrocyte-enriched cultures are not protected from apoptosis. (I) Protein lysates from CXCR2-sufficient and CXCR2-deficient oligodendrocyte cultures were assessed via western blot for total caspase 3, activated caspase 3, PARP, Bcl-2, and actin expression. NRS = normal rabbit serum treated mice. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to NRS-treated mice.