Fig. 9

Representative images of neocortex sections, double immunostained for GFAP and CCL2, from EAE-affected mice (a-f; cs 1.5, 2.0, 2.5, respectively) sacrificed at 6 h (a, d), 24 h (b, e), and 10 days (c, f) from disease onset and EAE-affected MSC-treated (g-i; cs 1.5) mice, sacrificed at 6 h after MSC treatment. a–c Astrogliosis and microgliosis in EAE-affected mice involve cortex parenchyma and microvessels (V); perineuronal (arrows) and perivascular (arrowheads) microglia processes prevail in cortex fields. d-f, (details of a-c, respectively) Laser confocal single optical planes show alternate astrocyte (d, arrowheads) and microglial cell perivascular processes (e, arrows); there is an extensive vessel coverage by microglia and double-layered perivascular sheathes (f, arrows); note in (e) the perivascular microglia (asterisk) and astrocyte (double asterisk) bodies. g In EAE-affected MSC-treated mice, even though hypertrophic perivascular microglial cells are still recognizable (arrows), astrogliosis is reduced and perivascular astrocytes prevail on the vessel wall (V). h, i details of g Laser confocal single optical planes show a few perivascular microglial cells (arrows) close to a continuous astrocyte cover (arrowheads); note in (i) a CCL2-reactive endothelial cell (asterisk). TOPRO-3 nuclear counterstaining. Scale bars: a–c, g 25 µm; d–f, h–i 10 µm