Diabetes impairs the late inflammatory response to wound healing

J Surg Res. 1991 Apr;50(4):308-13. doi: 10.1016/0022-4804(91)90196-s.


Diabetes mellitus is recognized as a risk factor for compromised wound healing. This study examines leukocyte infiltration and the appearance of tumor necrosis factor-alpha (TNF) and IL-6 in wound chambers implanted in normal and streptozotocin-induced diabetic mice. Perforated silicone wound chambers containing a strip of polyvinyl alcohol sponge were implanted along the flanks of normal and diabetic mice. Wound fluid aspirated from the chambers 1, 3, and 7 days following implantation was analyzed for the total number of leukocytes and TNF and IL-6 levels. While the number of leukocytes in the wound fluid was similar on Days 1 and 3 following implantation, there were significantly fewer inflammatory cells in wound fluid from diabetic animals (13.8 X 10(6)/ml) than in wound fluid from normal animals (28.5 Z 10(6)/ml) on Day 7 following implantation. TNF levels in the cell-free exudate fluid were similar between the two groups on all days examined. IL-6 levels were similar on Days 1 and 3 following implantation between the two groups, but there was significantly more IL-6 in wound fluid from normal animals (10,998 U/ml) than in wound fluid from diabetic animals (2096 U/ml) on Day 7 following implantation. Histologic evaluation of chambers 8 days following implantation revealed decreased neovascularization and less organization of granulation tissue. These data suggest that delayed healing in diabetes is associated with altered leukocyte infiltration and wound fluid IL-6 levels during the late inflammatory phase of wound healing.

MeSH terms

  • Animals
  • Diabetes Mellitus, Experimental / physiopathology*
  • Diffusion Chambers, Culture
  • Inflammation / physiopathology
  • Interleukin-6 / metabolism
  • Leukocytes / physiology
  • Mice
  • Mice, Inbred BALB C
  • Tumor Necrosis Factor-alpha / metabolism
  • Wound Healing*


  • Interleukin-6
  • Tumor Necrosis Factor-alpha