Figure 5.
Effects of macrophage depletion on the protection against sepsis elicited by interleukin 36α (IL-36α). A, Flow cytometry plots showed F4/80+ macrophages in the circulation isolated from spleens (n = 5 per group), at 48 hours after clodronate-encapsulated liposome treatment. †P < .001 (vs mice treated with phosphate-buffered saline [PBS]–encapsulated liposomes as a control; Mann–Whitney U test). B, C57BL/6 mice depleted of macrophages by clodronate liposomes were treated with or without recombinant mouse IL-36α, as in Figure 2B, after severe cecal ligation and puncture (CLP) with a 22-gauge needle, and survival was monitored. Comparison between groups was done by Kaplan–Meier analysis followed by log–rank tests. †P < .001 (vs mice treated with PBS liposomes as a control).

Effects of macrophage depletion on the protection against sepsis elicited by interleukin 36α (IL-36α). A, Flow cytometry plots showed F4/80+ macrophages in the circulation isolated from spleens (n = 5 per group), at 48 hours after clodronate-encapsulated liposome treatment. P < .001 (vs mice treated with phosphate-buffered saline [PBS]–encapsulated liposomes as a control; Mann–Whitney U test). B, C57BL/6 mice depleted of macrophages by clodronate liposomes were treated with or without recombinant mouse IL-36α, as in Figure 2B, after severe cecal ligation and puncture (CLP) with a 22-gauge needle, and survival was monitored. Comparison between groups was done by Kaplan–Meier analysis followed by log–rank tests. P < .001 (vs mice treated with PBS liposomes as a control).

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