Pathophysiological role of skin mast cells in wound healing after scald injury: study with mast cell-deficient W/W(V) mice.

BACKGROUND: The major role of mast cells in wound healing process has not been identified. In this study, we used mast cell-deficient W/W(V) mice and their congenic control (+/+) mice to examine the role of mast cells in scald wound healing.
METHODS: The size of the scald wound, thickness of the dermis, collagen deposition, vascularization, number of mast cells and chymase activity were measured before and at 3, 7, 14 and 21 days after inducing scald injury.
RESULTS: Although the process of wound closure and re-epithelialization was not markedly different between W/W(V) mice and +/+ mice, the degree of fibrous proliferation at the wound edge and wound vascularization in the proliferative phase was significantly lower in W/W(V) mice than in +/+ mice, and no vascular regression in the late remodeling phase was observed in W/W(V) mice. Mast cells producing chymase, FGF2, TGF-beta1 and VEGF were highly accumulated at the edge of scald wound in +/+ mice during the proliferative and remodeling phases at days 14 and 21. Chymase activity in the injured tissues of +/+ mice decreased in the acute phase, but recovered to no-injury level at days 14 and 21. The number of mast cells and chymase activity were very low in the injured tissues of W/W(V) mice throughout the experiment.
CONCLUSIONS: Wound healing after skin scald injury was partially impaired in mast cell-deficient mice. Mast cells may contribute to the wound healing process, especially in the proliferative and remodeling phases after scald injury.