Fig. 4.

GF mice have an altered inflammatory response following cuprizone-mediated demyelination. (A) GF mice and SPF controls were fed a diet containing 0.2% cuprizone for 5 wk from 8 wk of age. Mice were killed at the end of cuprizone administration, or after 3 wk of return to normal diet. A third group consisted of GF mice that were cohoused with SPF mice from 4 wk of age, becoming colonized with a microbiota after weaning. (B) PCR for a universal prokaryotic 16S sequence in fecal DNA, demonstrating absence of this amplicon in GF mice and its presence in the ex-GF group. (C) Representative images and (D) density of CD68^hi activated microglia/macrophages within the corpus callosum (yellow line) in cuprizone-naïve mice, following 5 wk cuprizone exposure (5w) and following a further 3 wk of normal diet (5+3w). (E) Representative images and density of (F) P2ry12^hiClec7a⁻ homeostatic and (G) P2ry12^loClec7a⁺ degeneration-associated microglia/macrophages within the corpus callosum. (Scale bars: C and E, 100 μm.) Error bars show mean ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001; 1-way ANOVA with Tukey HSD post hoc test, n = 4 to 5 mice.