Contribution of CARD9-mediated signaling to wound healing in skin

Abstract

The inflammatory response after skin injury involves the secretion of a variety of cytokines and growth factors that are necessary for tissue repair. Caspase recruitment domain-containing protein 9 (CARD9) is an essential signaling adaptor molecule for NF-κB activation upon triggering through C-type lectin receptors (CLRs), which are expressed in macrophages and dendritic cells. However, the role of CARD9 in inflammatory responses at the wound site has not been elucidated. In the present study, we analyzed the role of CARD9 in the healing process of skin wounds. Wounds were created on the backs of wild-type (WT) C57BL/6 mice and CARD9 gene-disrupted (knockout [KO]) mice. We analyzed percent wound closure, and the wound tissues were harvested for analysis of leukocyte accumulation and cytokine and chemokine expression. CARD9KO mice exhibited significant attenuation of wound closure compared with WT mice on days 5, 7, and 10 post-wounding, which was associated with decreased macrophage accumulation and reduced TNF-α, IL-1β, CCL3, and CCL4 expression. These results suggest that CARD9 may be involved in the wound healing process through the regulation of macrophage-mediated inflammatory responses.

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