Figure 4.
Type 1 IFN signaling mediates the activation of coagulation cascades in bacterial sepsis. (A-D) WT, IFN-α/βR1 KO, and TRIF KO mice subjected to either CLP or sham operation for 16 hours (WT group is the mixture of WT littermates of IFN-α/βR1 KO and TRIF KO mice). Thrombin and platelet fluorescence intensity in the liver microcirculation was quantified by using ImageJ software (A). Plasma levels of TAT complexes, PAI-1, fibrinogen (Fib), and D-dimer were measured (B). Representative images of immunohistochemical staining of fibrin in livers and lungs (×400) (C). Platelet counts in 16 hours after CLP- or sham-treated mice of indicated genotypes (D). (E) Kaplan-Meier survival plots for mice subjected to either CLP or sham operation (N = 11 mice per group). Data are shown as mean ± standard error of the mean. *P < .05; **P < .01. N = 4 to 11 mice per group.

Type 1 IFN signaling mediates the activation of coagulation cascades in bacterial sepsis. (A-D) WT, IFN-α/βR1 KO, and TRIF KO mice subjected to either CLP or sham operation for 16 hours (WT group is the mixture of WT littermates of IFN-α/βR1 KO and TRIF KO mice). Thrombin and platelet fluorescence intensity in the liver microcirculation was quantified by using ImageJ software (A). Plasma levels of TAT complexes, PAI-1, fibrinogen (Fib), and D-dimer were measured (B). Representative images of immunohistochemical staining of fibrin in livers and lungs (×400) (C). Platelet counts in 16 hours after CLP- or sham-treated mice of indicated genotypes (D). (E) Kaplan-Meier survival plots for mice subjected to either CLP or sham operation (N = 11 mice per group). Data are shown as mean ± standard error of the mean. *P < .05; **P < .01. N = 4 to 11 mice per group.

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