Fig. 5.

Deletion of CXCR3 significantly worsens survival to neonatal sepsis. Peritoneal granulocytes (Gr-1⁺ CD11b⁺) and macrophages (F4/80⁺ CD11b⁺) were collected from neonates at 0, 6, and 24 h postsepsis (LD₄₀) and stained for CXCR3 expression. Isotype controls are represented as dashed lines. Mean fluorescence intensity (MFI) of CXCR3 expression in granulocytes (A) and macrophages (B) was measured by flow cytometry (mean ± SDs; *, Dunn's one-way ANOVA, P < 0.05; **, Tukey's one-way ANOVA, P < 0.001; the figure represents the summary of two experiments [n = 6]). Peritoneal washes from wild-type (WT) or CXCR3^−/− neonates 12 h following an LD₄₀ CS challenge were harvested and analyzed via flow cytometry for the presence of granulocytes (C) or macrophages (D) (n = 4 per group; values represent the means ± SDs; *, Student's t test, P < 0.05). (E) Wild-type or CXCR3^−/− neonates were subjected an LD₄₀ septic challenge and then followed for survival for 7 days. The figure represents the summary of two experiments (n = 26; *, Fisher's exact test, P < 0.002).