The human burn wound as a primary source of interleukin-1 activity.

It has been suggested that interleukin 1 (IL-1) may be elevated systemically after major burn injury. Several metabolic changes commonly observed in patients with burns can be attributed in part to elevated IL-1 production; these include temperature elevation, skeletal muscle proteolysis, and alterations in the production of certain serum proteins by the hepatocyte (e.g., albumin and acute phase reactants). In this article we describe a likely source of this elevated IL-1 activity: the burn wound. Fluid taken from blisters on thermally injured skin early after burn injury contains substantial amounts of IL-1. This activity is less apparent in certain blister fluid (BF) samples, probably because of the presence of an inhibitor(s) of lymphocyte proliferation. However, after gel filtration high-performance liquid chromatography, the IL-1 actively elutes at a molecular weight of 15,000 to 20,000 daltons and can be blocked with an antibody to IL-1. We suggest that the source of this IL-1 activity is the injured keratinocyte and that release of this IL-1 systemically is inevitable. We postulate that release of IL-1 from the wound into the systemic circulation accounts in part for the metabolic changes outlined above. Furthermore, since epidermal IL-1 is a potent T cell chemoattractant, we believe that burn wound IL-1 may affect sequestration of T cells near the burn wound, resulting in T cell lymphopenia.