Fig. 4.

SAgs promote pathogenic production of IFN-γ that supports bacterial burden. (A) DR4-B6 mice were inoculated i.v. with wild-type S. aureus COL or the COL Δseb deletion strain. At 24 hpi, animals were killed, livers and blood were harvested, and material was prepared for IFN-γ analysis. Each dot represents an individual mouse, the bar indicates the geometric mean, and error bars indicate the SD. The dotted line indicates the levels detected in an uninfected animal. (B) B6 and DR4-B6 mice were treated 18 h prior to infection with 250 µg isotype control or αIFN-γ antibody administered by i.p. injection and animals were infected i.v. with wild-type S. aureus COL or COL Δseb. (C) DR4-B6 animals were treated with 20 µg (40 µg total) recombinant murine IFN-γ or vehicle control (100 µL PBS) i.p. 2 h before and 1 h after i.v. infection with S. aureus COL Δseb. In both experiments (B and C), in vivo bacterial burden was assessed after 96 h in liver and kidneys and an assessment of gross pathological liver lesions was also performed. Each dot represents an individual mouse, and the bar indicates the geometric mean for CFUs/organ and the median for lesions/organ. Significant differences were determined using the Mann–Whitney U test or Kruskal–Wallis test with the uncorrected Dunn’s test for multiple comparisons (*P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001).