Fig. 5

Neuronal IKKβ promotes astrocyte and microglia responses and inflammatory mediators in CPZ demyelination. (Ai) Iba1 immunostaining of microglia and (Di) GFAP immunostaining of astrocytes in serial brain coronal paraffin sections from nIKKβKO and IKKβff control naïve (CPZ0) or CPZ-fed CPZ3 and CPZ5 mice. Scale bars: 100 μM. Quantitative representation of areas covered by (Aii) Iba1 immunoreactivity and (Dii) GFAP immunoreactivity in the medial corpus callosum in groups of nIKKβKO and IKKβff control mice represented in the photographs. (B, C, and E) Differential expression of the inflammatory marker genes Tnf, Ccl2, and Cxcl16 relative to GusB in total mRNA isolates taken from nIKKβKO and IKKβff control brains from CPZ0 or CPZ-fed CPZ2, CPZ3, CPZ5, CPZ6+0.5, CPZ6+1, and CPZ6+4 mice. Results are means of 2 (nIKKβKO CPZ6+0.5, CPZ6+1, nIKKβKO CPZ6+4) or 3–5 mice (for all other groups and time points) from one representative of two independent experiments. The most relevant statistically significant differences after comparisons between groups are shown by Student’s t-test (Aii and Dii) and by two-way ANOVA with Bonferroni’s test (B, C, and E). *p ≤ 0.05, **p ≤ 0.005, ***p ≤ 0.001