Mast cell involvement in normal human skin wound healing: expression of monocyte chemoattractant protein-1 is correlated with recruitment of mast cells which synthesize interleukin-4 in vivo

J Pathol. 2000 Jan;190(1):100-6. doi: 10.1002/(SICI)1096-9896(200001)190:1<100::AID-PATH496>3.0.CO;2-Q.


Mast cells (MCs) are known as key cells of immediate type hypersensitivity reactions. It has recently been shown that MCs regulate fibroblast proliferation by heterotypic cell-cell contact and secretion of interleukin-4 (IL-4) in vitro. It was therefore hypothesized that MCs may contribute to wound repair in vivo. Using immunohistology and in situ hybridization, the time course of mast cell recruitment and the expression of MC-attractant chemokines were analysed in a human skin wound-healing model, and the production of IL-4 by MCs in vivo was investigated. The data obtained indicate that the five-fold increase of the tryptase+ MCs at the fibrotic border of the wound within the first 10 days is the result of increased recruitment/survival of MCs or MC precursors, but not of increased local proliferation. Recruitment of MCs is paralleled by the expression of monocyte chemoattractant protein-1 (MCP-1), but not by other chemokines such as RANTES (regulated on activation, normal T cell expressed and secreted) and/or MIP (macrophage inflammatory protein)-1alpha/beta. Notably, 60-70% of MCs exhibited strong and selective IL-4 immunoreactivity, whereas other resident and passenger cells were rather quiescent. The data suggest that MC contribute significantly to the cytokine network of wound repair via MC-derived IL-4 and stimulation of fibroblast proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cell Count
  • Chemokine CCL2 / analysis*
  • Chemokine CCL2 / genetics
  • Chemotaxis
  • Chymases
  • Humans
  • Immunohistochemistry
  • In Situ Hybridization
  • Inflammation Mediators / analysis
  • Interleukin-4 / analysis*
  • Interleukin-4 / genetics
  • Keratinocytes / metabolism
  • Macrophages / metabolism
  • Mast Cells / metabolism*
  • Mast Cells / pathology
  • Microscopy, Interference
  • RNA, Messenger / analysis
  • Serine Endopeptidases / analysis
  • Skin / metabolism*
  • Skin / pathology
  • Tryptases
  • Wound Healing*


  • Chemokine CCL2
  • Inflammation Mediators
  • RNA, Messenger
  • Interleukin-4
  • Serine Endopeptidases
  • chymase 2
  • Chymases
  • Tryptases