Figure 4.
Lack of microbes enhances microglia immune response. (a) Representative IHC images of OB, CC, and P/M/C tissue from Ctrl, ABX, HSV-1-infected normal or ABX-treated mice, respectively. Increased Iba-1 staining indicated that HSV-1 infection triggers the transformation from resting microglia to activated microglia, whereas ABX pretreatment induces the microglia to a form with increased cytokine production. Number of Iba-1+ ramified parenchymal microglia (active microglia) and microglia in “increased cytokine production” form in different localizations of the CNS were calculated. At least three sections per mouse were examined. Data are presented as mean ± SD. *p< .05 or **p < .01 versus HSV-1 group. (b) Total RNA of sorted mouse CD11b+ CD45lo microglia was extracted and the mRNA expression profile was analyzed by RNA-seq. The differentially expressed genes (at least 2-fold, p < .05 in HSV-1 compared with ctrl microglia) were enriched in several key cellular functions, components and biological progresses by Gene Ontology (GO) analysis. (c) Heat map of the expression of microglia activation-related gene transcripts (1.5-fold, p < .05, unpaired t test) in sorted microglia from normal, ABX, HSV-1 and ABX + HSV-1 mice. Color code presents linear values. (d) mRNA expression values (log2 fold change vs Ctrl group) of genes from microglia in Ctrl, HSV-1 or HSV-1+ ABX mice were categorized according to the M0, M1 or M2 phenotypes, as described previously.27