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. 2013 May 9;9(5):e1003351. doi: 10.1371/journal.ppat.1003351

Figure 6. SB203580, an RIP2 inhibitor downstream of nucleotide-binding oligomerization domain (NOD)2, attenuates CLP-induced sepsis.

Figure 6

(A) Peritoneal cells of WT mice were cultured with SB203580 and/or MDP for 24 h, and IL-1β and IL-10 concentrations were measured in culture fractions. (B) Molecules related to NOD2-mediated signal transduction were blotted using peritoneal cells obtained from WT and Nod2−/− mice injected with SB203580 or PBS 24 h after CLP. (C) Serum and peritoneal IL-1β, IL-10, and C5a levels were estimated in WT (n = 4) and Nod2−/− (n = 3) mice injected with SB203580 (n = 4 in WT, n = 3 in Nod2−/−) or PBS 24 h after CLP by ELISA. (D) The levels of CD55 expression on F4/80−Ly6-G+ cells from WT (n = 3) and WT mice injected with SB203580 (n = 3) were measured 24 h after CLP. (mean fluorescence intensity [MFI] of CD55 expression in the panels, diagrams filled with gray for istotype-matched control IgG, solid lines for CD55) (E) The percentages of surviving mice were estimated during CLP-induced sepsis (aP = 0.0312, log-rank test, n = 6–8 per group; WT mice injected with SB203580 vs. PBS). *P<0.05, **P<0.01, ***P<0.001 (two-tailed unpaired t-test [a, c]). Results shown are representative of three independent experiments except for (E) (mean and SEM).