Fig. 3: Super-affinity IL-1Ra accelerates wound healing in diabetic mice.

a, b Full-thickness wounds in Lepr^db/db were treated with IL-1Ra or PDGF-BB variants (0.5 μg of wild types, equimolar of engineered versions). Wound closure evaluated by histomorphometric analysis of tissue sections in (a). n = 8 wounds per condition. Representative histology (haematoxylin and eosin staining) 9 days post treatment shown in (b). 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. c, d Angiogenesis at day 9 assessed by immunostaining of wound sections for CD31 (endothelial cells, red) and desmin (smooth muscle cells, green). Representative images in (c). Dashed lines indicate separation between epidermis (indicated as e) and dermis (indicated as d). Scale bar = 0.2 mm. Quantification of CD31 in (d). n = 8. e Schematic representation of hypothesised IL-1Ra/PlGF_123–141 effects in diabetic wounds. MΦs macrophages, MMPs matrix metallopeptidases, SASP senescence-associated secretory phenotype; grey arrows represent induction; blue lines represent inhibition. f Neutrophil and macrophage populations in wounds measured by flow cytometry at various time points post wounding. Percentages were calculated over total live wound cells. Median fluorescence intensity (MFI) for CD206 was measured in macrophages (F4/80⁺, CD11b⁺ cells). n = 8 wounds. In (a), (d) and (f), data are means ± SEM. One-way ANOVA with Bonferroni post hoc test for pair-wise comparisons (significances shown are between saline and the other groups, unless indicated otherwise). *P ≤ 0.05, **P ≤ 0.001, ***P ≤ 0.001. ns non-significant.