Fig. 5

CMH promotes increased laminin expression in the vascular basement membrane. a-c. Frozen sections of lumbar spinal cord taken from EAE-normoxia or EAE-CMH mice at the peak symptomatic phase of EAE were stained for CD45 (AlexaFluor-488) and laminin (Cy-3) in panel A, CD31 (AlexaFluor-488) and laminin (Cy-3) in panel B or CD45 (AlexaFluor-488) and laminin (Cy-3) in panel C. Scale bar = 50 μm. Note that in EAE, infiltrating leukocytes accumulate in the perivascular space between the endothelial and parenchymal layers of the vascular basement membrane, causing them to separate (a). In B note that only the inner layer of basement membrane co-localizes with CD31. In C note that while in the normoxic EAE spinal cord, leukocytes break through the basement membrane to migrate freely into the CNS parenchyma, CMH-treated mice showed a thicker stronger expression of laminin in the basement membrane, resulting in greater containment of leukocytes within perivascular cuffs. d. Quantification of vascular laminin expression. Results are expressed as the mean ± SEM (n = 6 mice/group). Note that CMH enhanced laminin expression within the parenchymal basement membrane. ** p < 0.01