Defect of Dectin-1-mediated signaling promotes burn wound healing through attenuated oxidative stress and inflammatory responses.

BACKGROUND

In burn wound healing, inflammation and oxidative stress are major contributors to delayed repair. Damage-associated molecular patterns (DAMPs) derived from injured tissue activate inflammatory signaling pathways through receptors, such as C-type lectin receptors (CLRs). Dectin-1, one of the receptors for DAMPs, contributes to the production of inflammatory cytokines and reactive oxygen species (ROS). The purpose of this study was to investigate the role of Dectin-1 in burn wound healing using Dectin-1-deficient (KO) mice and the antagonist laminarin.

METHOD: Full-thickness burn wounds were created on the dorsal skin of wild-type (WT) C57BL/6 mice and Dectin-1KO mice by applying a 90°C soldering iron for 10 s. We analyzed the percentage of wound closure, the area of granulation tissue, angiogenesis, and inflammatory responses. To evaluate the effect of the topical administration of the Dectin-1 antagonist laminarin, we applied laminarin or vehicle at the burned sites daily and examined burn wound healing.

RESULTS

The percentages of wound closure, granulation tissue area, and angiogenesis were significantly enhanced in Dectin-1KO mice compared with WT mice. Dectin-1 deficiency also led to reduced production of inflammatory cytokines such as TNF-α and IFN-γ, and the oxidative damage marker 4-HNE. Furthermore, daily topical administration of the antagonist laminarin promoted burn wound healing.

CONCLUSIONS

These results suggest that Dectin-1-mediated signaling inhibits burn wound healing by inducing the production of inflammatory cytokines and oxidative stress. Furthermore, topical administration of the Dectin-1 antagonist laminarin may serve as a promising novel treatment for healing after burn.