Inhibition of CXCL10 abolishes protective adjuvant effect of a TLR4 agonist in response to sepsis, and CXCL10 administration modestly improves survival to sepsis. Sera (A) or peritoneal washes (B) were collected from neonates at multiple time points postsepsis and assayed via ELISA for the concentration of CXCL10. The dashed line represents the concentrations of CXCL10 from naïve animals following septic challenge. (C to E) Two hours prior to LPS or saline administration, animals were administered either anti-CXCL10 or control IgG (0.5 mg). Twenty-four hours following LPS administration, peritoneal washes were harvested and cells were stained for granulocytes (C) (Gr-1+ CD11b+) and macrophages (D) (F4/80+ CD11b+) and analyzed by flow cytometry. The figure represents the summary of three experiments (*, Student's t test, P < 0.05; error bars indicate SDs). (E) Twenty-four hours following LPS or saline pretreatment, neonates were challenged with an LD70 sepsis and then followed for survival. The figure represents the summary of two experiments (*, Fisher's exact test comparing control IgG+LPS and anti-CXCL10–LPS, P < 0.001). (F) Twelve hours prior to sepsis, neonates were administered either recombinant murine CXCL10 (rCXCL10; 20 ng) or physiologic saline. Following sepsis, animals were then followed for survival for 7 days. The figure represents the summary of three experiments (*, Fisher's exact test, P = 0.066).