Figure 4.

LCN2 upregulation following S. epidermidis infection in the neonatal hippocampus is independent of genetic attenuation of reactive gliosis

(A–C) Representative images of astrocyte cell soma (100× oil immersion objective lens) in sections stained with GFAP of saline (left) and S. epidermidis (right) mice. GFAP positive astrocyte cell soma was measured in the MDG (B) and CA1SR (C) hippocampal subregion 24 h after S. epidermidis infection.

(D–F) Hippocampal protein levels of lcn2 24 h after S. epidermidis infection (saline WT n = 8, S. epidermidis WT n = 11, saline GFAP^−/−Vim^−/− n = 11, S. epidermidis GFAP^−/−Vim^−/− n = 11). PND4 WT and GFAP^−/−Vim^−/− pups were injected with S. epidermidis and subjected to hypoxia-ischemia 24h later. Hippocampal gray matter (E) and white matter (F) brain injury was assessed using microtubule-associated protein 2 (MAP-2) and myelin basic protein (MBP) staining respectively (S. epidermidis WT n = 7, S. epidermidis GFAP^−/−Vim^−/− n = 6).

(G) Representative images (4× objective lens) of PND14 GFAP^−/−Vim^−/− and WT male mice brain sections stained with MAP-2 and MBP following S. epidermidis injection at PND4 in combination with hypoxia-ischemia 24h later. Data are presented as median, 10–90th percentile. Statistical comparison between S. epidermidis and saline for each group was performed using two-way ANOVA with Tukey’s multiple comparison post-hoc test or independent t-test. ∗∗p < 0.01; ∗∗∗p < 0.001 (see also Figure S2).