Figure 4.
Caspase-11 deletion prevents NET release and organ dysfunction during polymicrobial sepsis. (A) Circulating amounts of MPO/DNA-NETs were quantified 24 hours after sepsis induction by CLP. (B-F) Plasma levels of organ injury markers. (G) Representative images of H&E staining of lung tissue sections from WT and Casp11−/− mice 24 hours after sepsis induction by CLP are shown at ×200 magnification. The square insets represent the image at ×400 magnification. (H-J) The plasma levels of the cytokines TNF-α, IL-6, and IL-1β (G-I) were determined 24 hours after sepsis induction by CLP. (K-L) WT and Casp11−/− mice were implanted using a telemetric pressure transmitter probe to determine the MAP and HR 24 hours after CLP-induced sepsis. The data are expressed as means ± SEM. *P < .05; 1-way ANOVA followed by Tukey’s test (A-F,H-J), CLP WT vs CLP Casp11−/− Student t test (K,L). The data are representative of ≥ 2 independent experiments, each including 4 to 7 animals per group.

Caspase-11 deletion prevents NET release and organ dysfunction during polymicrobial sepsis. (A) Circulating amounts of MPO/DNA-NETs were quantified 24 hours after sepsis induction by CLP. (B-F) Plasma levels of organ injury markers. (G) Representative images of H&E staining of lung tissue sections from WT and Casp11−/− mice 24 hours after sepsis induction by CLP are shown at ×200 magnification. The square insets represent the image at ×400 magnification. (H-J) The plasma levels of the cytokines TNF-α, IL-6, and IL-1β (G-I) were determined 24 hours after sepsis induction by CLP. (K-L) WT and Casp11−/− mice were implanted using a telemetric pressure transmitter probe to determine the MAP and HR 24 hours after CLP-induced sepsis. The data are expressed as means ± SEM. *P < .05; 1-way ANOVA followed by Tukey’s test (A-F,H-J), CLP WT vs CLP Casp11−/− Student t test (K,L). The data are representative of ≥ 2 independent experiments, each including 4 to 7 animals per group.

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