Fig. 5: MC activation mediates macrovascular dilation and endovascular leakage in septic shock.

Rectal temperature A in WT (n = 8) or MC-deficient mice (Kit^W-sh; n = 6), and B in MC-depleted mice (MCPT5-DTA; n = 12) or non-depleted littermate controls (n = 7) after injection of 4 × 10⁸ colony forming units/ml (CFU) E. coli J96, or C in MC-depleted mice (MCPT5-DTA; n = 5) and non-depleted littermate controls (n = 5) in a CLP sepsis model. D Tracings of the mean arterial pressure after injection of saline (Sham; n = 5) or of 4 × 10⁸ CFU E. coli J96 in WT (WT Shock; n = 5) and in MC-deficient mice (Kit^W-sh Shock; n = 5). Additionally, WT mice pretreated with the MC inhibitor Ketotifen were injected with 4 × 10⁸ CFU E. coli J96 (Ketotifen Shock; n = 5). E Hematoxylin Eosin staining of lungs 1 hour after injection of saline (Sham) or 4 × 10⁸ CFU E. coli J96 into WT (WT Shock) or MC-deficient mice (Kit^W-sh Shock). Images representative of experiments in 6 mice/condition. Arrows highlight intraalveolar fluid. Scale bars: 100 µm. F Measurement of Evans Blue extravasation in indicated organs after i.v. injection of saline (n = 6) or 4 × 10⁸ CFU E. coli J96 in WT (n = 12) or Kit^W-sh mice (n = 6). ns= non significant, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 by one- or two-way ANOVA with Tukey’s multiple comparisons test as appropriate. All data are shown as mean ± SEM. Source data including exact p values are provided as a Source Data file.