Fig. 1: IL-1R1 signalling delays wound healing in diabetic mice.

a Full-thickness wounds (5 mm) were created in diabetic mice (Lepr^db/db) and non-diabetic littermates (Lepr^db/+). Concentrations of IL-1β and IL-1Ra in wounds harvested at various time points. n = 4 wounds per time point. b Concentrations of IL-1β detected in media of unstimulated or stimulated (LPS + ATP) bone marrow-derived macrophages (MΦs) from Lepr^db/+ and Lepr^db/db mice. c Lepr^db/db mice were crossed with Il1r1^−/− mice to generate diabetic mice deficient for IL-1R1. Representative pictures of 14-week-old mice are shown. Scale bar = 1 cm. d, e Full-thickness wounds were created in Lepr^db/db and Lepr^db/db-Il1r1^−/− mice. Graph in d shows wound closure kinetics evaluated by histomorphometric analysis of tissue sections. n = 12 wounds per time point. Representative histology (haematoxylin and eosin staining) after 9 days are shown in (e). Black arrows indicate wound edges and red arrows indicate tips of epithelium tongue. The epithelium (if any) appears in purple as a homogeneous keratinocyte layer on top of the wounds. The granulation tissue under the epithelium contains granulocytes with dark-purple nuclei. Fat tissue appears as transparent bubbles. Scale bar = 1 mm. For (a), (b) and (c), data are means ± SEM. For (a) and (d), two-way ANOVA with Bonferroni post hoc test for pair-wise comparisons. For (b), two-tailed Student’s t test. **P ≤ 0.01, ***P ≤ 0.001.