Mast cells are traditionally viewed as effector cells of immediate type
hypersensitivity reactions. There is, however, a growing body of evidence that the cells might play an important role in the maintenance of tissue homeostasis and repair. We here present our own data and those from the literature elucidating the possible role of mast cells during wound healing. Studies on the fate of mast cells in
scars of varying ages suggest that these cells degranulate during wounding, with a marked decrease of
chymase-positive cells, although the total number of cells does not decrease, based on
SCF-receptor staining. Mast cells contain a plethora of preformed mediators like
heparin,
histamine,
tryptase,
chymase,
VEGF and
TNF-alpha which, on release during the initial stages of wound healing, affect
bleeding and subsequent coagulation and acute
inflammation. Various additional vasoactive and chemotactic, rapidly generated mediators (C3a, C5a,
LTB4,
LTC4, PAF) will contribute to these processes, whereas mast cell-derived proinflammatory and growth promoting
peptide mediators (
VEGF,
FGF-2, PDGF,
TGF-beta,
NGF, IL-4, IL-8) contribute to neoangiogenesis, fibrinogenesis or re-epithelization during the repair process. The increasing number of
tryptase-positive mast cells in older
scars suggest that these cells continue to be exposed to specific chemotactic, growth- and differentiation-promoting factors throughout the process of tissue remodelling. All these data indicate that mast cells contribute in a major way to wound healing. their role as potential initiators of or as contributors to this process, compared to other cell types, will however have to be further elucidated.