Jameson et al. noted that nonhealing wounds in DETC-deficient mice were less inflamed than normal wounds. They now show that, though neutrophils arrived at the wound on schedule, macrophages showed up late. The macrophage tardiness could be traced back to the lack of FGF-7. In normal wounds, FGF-7 was found to trigger the production of hyaluronan by neighboring keratinocytes and hyaluronan was needed to recruit macrophages. If hyaluronan (or FGF-7) was added back to the wounds, the macrophages returned and healing was restored.
Impaired wound healing is prevalent in patients with diabetes and rheumatoid arthritis. The authors hope to investigate whether impaired DETC function may be to blame in these human diseases.