Figure 1. HK is selectively required for LPS-induced mortality in mice. (A–D) LPS from E. coli 055:B5 was injected i.p. into Kng1−/−, Klkb1−/−, FXII−/−, or B1RB2R−/− mice and their WT littermates (control) at a dose of 50 mg/kg body weight (n = 15 mice/group), respectively. The survival rate was monitored and analyzed using a log-rank test. **, P < 0.01. (E and F) Kng1−/− mice and their WT littermates (control) were challenged by i.p. injection of 0.5 mg/kg murine TNF (E; n = 10), or by d-galactosamine (15 mg/mouse) pretreatment (i.p.) plus polyinosinic:polycytidylic acid (30 µg/mouse) treatment (i.v.; F; n = 10), and their survival rate was monitored. Statistics were analyzed using a log-rank test. Data are representative of two (B–F) or three (A) independent experiments.
Figure 1.

HK is selectively required for LPS-induced mortality in mice. (A–D) LPS from E. coli 055:B5 was injected i.p. into Kng1−/−, Klkb1−/−, FXII−/−, or B1RB2R−/− mice and their WT littermates (control) at a dose of 50 mg/kg body weight (n = 15 mice/group), respectively. The survival rate was monitored and analyzed using a log-rank test. **, P < 0.01. (E and F) Kng1−/− mice and their WT littermates (control) were challenged by i.p. injection of 0.5 mg/kg murine TNF (E; n = 10), or by d-galactosamine (15 mg/mouse) pretreatment (i.p.) plus polyinosinic:polycytidylic acid (30 µg/mouse) treatment (i.v.; F; n = 10), and their survival rate was monitored. Statistics were analyzed using a log-rank test. Data are representative of two (B–F) or three (A) independent experiments.

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