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Fig. 5 | Fluids and Barriers of the CNS

Fig. 5

From: Microglia-derived CCL2 has a prime role in neocortex neuroinflammation

Fig. 5

Representative images of neocortex sections from naïve (a, d, g), EAE-affected (b, e, h; cs 1.5, 2.0, 2.5, respectively), and EAE-affected MSC-treated (c, f, i; cs 1.0, 1.5, 2.0, respectively) mice, sacrificed at 6 h (a–c), 24 h (d–f), and 10 days (g–i) after MSC treatment, double immunostained for TMEM119 and CCL2. a, d, g In naïve mice, the typical delicate morphology of surveillant microglia is revealed by TMEM119 staining of cell bodies (arrows) and processes (arrowheads). b, e, h In EAE mice, TMEM119 is extensively colocalized with CCL2 on hypertrophic microglial cells, with the chemokine staining largely prevailing on cell bodies and processes (yellowish/reddish fluorescence; arrows). c, f, i Microglia hypertrophy and CCL2 staining are reduced on microglia of EAE-affected MSC-treated mice, with reduced cell points of CCL2/TMEM119 colocalization (yellowish fluorescence) and a prevailing TMEM119 staining (green fluorescence; arrows); note in (i) TMEM119-positive microglia processes that surround the wall of a cortex microvessel (V, arrowheads). TOPRO-3 nuclear counterstaining. Scale bars: a–i 20 µm

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