Advertisement
Research Article| Volume 50, ISSUE 4, P308-313, April 1991

Download started.

Ok

Diabetes impairs the late inflammatory response to wound healing

DOI:https://doi.org/10.1016/0022-4804(91)90196-S
Diabetes impairs the late inflammatory response to wound healing
Previous ArticleLeukotriene C4 induces mesenteric hypoperfusion and intestinal intramural acidosis in pigs
Next ArticleMetabolic inhibition potentiates oxidant injury
      This paper is only available as a PDF. To read, Please Download here.

      Abstract

      Diabetes mellitus is recognized as a risk factor for compromised wound healing. This study examines leukocyte infiltration and the appearance of tumor necrosis factor-α (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 × 106/ml) than in wound fluid from normal animals (28.5 × 106/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.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Journal of Surgical Research
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Register: Create an account
      Institutional Access: Sign in to ScienceDirect

      References

        • Spanheimer R.G.
        • Umpierrez G.E.
        • Stumpf V.
        Decreased collagen production in diabetic rats.
        Diabetes. 1988; 37: 371
        • Yue D.K.
        • McLennan S.
        • Marsh M.
        • Mai Y.W.
        • Spalviero J.
        • Delbridge L.
        • Reeve T.
        • Turtle J.R.
        Effects of experimental diabetes, uremia, and malnutrition on wound healing.
        Diabetes. 1987; 36: 295
        • Goodson W.H.
        • Hunt T.K.
        Wound collagen accumulation in obese hyperglycemic mice.
        Diabetes. 1986; 35: 491
        • Spanheimer R.G.
        Direct inhibition of collagen production in vitro by diabetic rat serum.
        Metabolism. 1988; 37: 479
        • Goodson W.H.
        • Hunt T.K.
        Studies of wound healing in experimental diabetes mellitus.
        J. Surg. Res. 1977; 22: 221
        • Fahey III, T.J.
        • Sherry B.
        • Tracey K.J.
        • van Deventer S.
        • Jones W.G.
        • Minei J.P.
        • Morgello S.
        • Shires G.T.
        • Cerami A.
        Cytokine production in a model of wound healing: The appearance of MIP-1, MIP-2, cachectin/TNF and IL-1.
        Cytokine. 1990; 2: 92
        • Ford H.R.
        • Hoffman R.A.
        • Wing E.J.
        • Magee D.M.
        • McIntyre L.
        • Simmons R.L.
        Characterization of wound cytokines in the sponge matrix model.
        Arch. Surg. 1989; 124: 1422
        • Leibovich S.J.
        • Polverini P.J.
        • Shepard H.M.
        • Wiseman D.M.
        • Shively V.
        • Nuseir N.
        Macrophage-induced angiogenesis is mediated by tumor necrosis factor-α.
        Nature. 1987; 329: 630
        • Kohase M.
        • Henriksen-Destefano D.
        • Sehgal P.B.
        • Vilcek J.
        Dexamethasone inhibits feedback regulation of the mitogenic activity of tumor necrosis factor, interleukin-1 and epidermal growth factor in human fibroblasts.
        J. Cell. Physiol. 1987; 132: 271
        • Kishimoto T.
        The biology of interleukin 6.
        Blood. 1989; 74: 1
        • Diegelmann R.F.
        • Lindblad W.J.
        • Cohen I.K.
        A subcutaneous implant for wound healing studies in humans.
        J. Surg. Res. 1986; 40: 229
        • Mosmann T.
        Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays.
        J. Immunol. Methods. 1983; 65: 55
        • Andreassen T.T.
        • Oxlund H.
        The influence of experimental diabetes and insulin treatments on the biomechanical properties of rat skin incisional wounds.
        Acta Chir. Scand. 1987; 153: 405
        • Hennessey P.J.
        • Ford E.G.
        • Black C.T.
        • Andrassy R.J.
        Wound collagenase activity correlates directly with collagen glycosylation in diabetic rats.
        J. Pediatr. Surg. 1990; 25: 75
        • Goodson III, W.H.
        • Hunt T.K.
        Wound healing and the diabetic patient.
        Surg. Gynecol. Obstet. 1979; 149: 600
        • McMurry Jr., J.F.
        Wound healing with diabetes mellitus: Better glucose control for better wound healing in diabetes.
        Surg. Clin. North Am. 1984; 64: 769
        • Mowat A.G.
        • Baum J.
        Chemotaxis of polymorphonuclear leukocytes from patients with diabetes mellitus.
        N. Engl. J. Med. 1971; 284: 621
        • Pereira M.A.
        • Sannomiya P.
        • Garcia-Leme J.
        Inhibition of leukocyte chemotaxis by a factor in alloxan-induced diabetic rat plasma.
        Diabetes. 1987; 36: 1307
        • Sannomiya P.
        • Pereira M.A.
        • Garcia-Leme J.
        Inhibition of leukocyte chemotaxis by serum factor in diabetes mellitus: Selective depression of cell responses mediated by complement-derived chemoattractants.
        Agents Actions. 1990; 30: 369
        • Bybee J.D.
        • Rogers D.E.
        The phagocytic activity of polymorphonuclear leukocytes obtained from patients with diabetes mellitus.
        J. Lab. Clin. Med. 1964; 64: 1
        • Drachman R.H.
        • Root R.K.
        • Wood Jr., W.B.
        Studies of the effect of experimental nonketotic diabetes mellitus on antibacterial defense. I. Demonstration of a defect in phagocytosis.
        J. Exp. Med. 1966; 124: 227
        • Steenfos H.H.
        • Hunt T.K.
        • Scheuenstuhl H.
        • Goodson III, W.H.
        Selective effects of tumor necrosis factor-α on wound healing in rats.
        Surgery. 1989; 106: 171
        • Mahadevan V.
        • Hart I.R.
        • Lewis G.P.
        Factors influencing blood supply in wound granulomas quantitated by a new in vivo technique.
        Cancer Res. 1989; 49: 415
        • Lorenzi M.
        • Nordberg J.A.
        • Toledo S.
        High glucose prolongs cell-cycle traversal of cultured human endothelial cells.
        Diabetes. 1987; 36: 1261

      Article info

      Publication history

      Presented at the Annual Meeting of the Association for Academic Surgery, Houston, Texas, November 14–17, 1990

      Identification

      DOI: https://doi.org/10.1016/0022-4804(91)90196-S

      Copyright

      © 1991 Published by Elsevier Inc.

      ScienceDirect

      Access this article on ScienceDirect

      The content on this site is intended for healthcare professionals.


      We use cookies to help provide and enhance our service and tailor content. To update your cookie settings, please visit the Cookie Preference Center for this site.
      Copyright © 2023 Elsevier Inc. except certain content provided by third parties.


      RELX