Impaired cutaneous wound healing in interleukin-6 deficient mice.
Gallucci-RM; Simeonova-PP; Matheson-JM; Kommineni-C; Guriel-JL; Sugawara-T; Luster-MI
FASEB J 2000 Apr; 14(6)(Suppl S):A1110
It is well known that the inflammatory response following cutaneous wounding is necessary for healing, and it has been postulated that inflammatory cytokines, such as IL-6, might be intimately involved in the healing process. However, studies concerning the exact role of this cytokine during wound healing are unclear. When subject to full thickness cutaneous wounds, IL6 deficient mice displayed significantly delayed healing compared to control animals. Histology of wounds from IL6 deficient mice displayed no epithelial bridge formation, minimal granulation tissue formation and little inflammation. IL6 mRNA was expressed in the epidermis of the leading edge of the wound, in dermal fibroblasts, and macrophages in wildtype mice, but not in IL6 deficient mice. Mobility shift assays of skin samples from wildtype and IL6 deficient mice showed decreased AP-1 induction 16 hours post wounding. When IL6 deficient mice were treated with a single dose of recombinant IL6 they displayed healing virtually indistinguishable from wildtype mice. Gene replacement treatment, utilizing a plasmid construct containing the murine IL6 gene, of IL6 deficient mice produced results similar to treatment with recombinant IL6.
Laboratory-animals; Animals; Animal-studies; Injuries; Health-care; Occupational-health
Toxicology and Molecular Biology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health MS 3014, 1095 Willowdale Rd., Morgantown, WV 26505, USA
Abstract; Conference/Symposia Proceedings
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