Figure 4.
Effect of −30 h KRN treatment on invariant natural killer T (iNKT) activation cell activation and survival in septic neonatal mice. Neonatal C57BL/6 pups received KRN (0.2 µg/g BW) or vehicle (2.5% dimethyl sulfoxide in PBS) intraperitoneal (i.p.) 30 h prior to (−30 h K) sepsis induction. Sepsis was then induced by i.p. injection of cecal slurry (CS, 0.9 mg/g BW). Serum and liver were harvested 10 h later. (A) Representative histogram of CD69 expression on hepatic iNKT cells. (B) Flow cytometric analysis of surface CD69 expression on gated hepatic iNKT cells. (C) Interferon (IFN)-γ levels in the serum were measured by enzyme-linked immunosorbent assay. Data expressed as mean ± SEM (n = 5–9 per group) and compared by one-way analysis of variance (*p < 0.05 vs. Sham, #p < 0.05 vs. Vehicle). (D) Another set of pups received the same dose of KRN or vehicle 30 h prior to sepsis induction by CS (0.175 mg/g) and survival was monitored for 7 days (n = 15–16 per group, *p = 0.026 vs. Vehicle, log-rank test).