THERMAL-INJURY INDUCES VERY EARLY PRODUCTION OF INTERLEUKIN-1-ALPHA IN THE RAT BY MECHANISMS OTHER THAN ENDOTOXEMIA

Background. Cytokines are putative mediators of thermal injury-induced systemic changes. We studied the effects of thermal injury on cytokin e activation in vivo with a sensitive radioimmunoassay specific for ra t interleukin-1 alpha (IL-1 alpha). Methods. We characterized the orga n distribution and expression kinetics of IL-1 alpha in rats submitted to either 20% total body surface area cutaneous born, muscle born, or endotoxic shock. Rats were killed at various time points, and liver, lung, spleen, ileum, thymus, kidney, skin, and plasma were harvested. Tissues were homogenized, and the supernates were assayed for rat IL-1 alpha. The assay detection limit was 1.5 ng/gm wet tissue (WT). Resul ts. Thermal injury induced marked elevations of IL-1 alpha levels in t he liver and injury, and maximal levels were reached at 2.5 hours when compared with controls. In the liver mean IL-1 alpha levels in cutane ous burn injury were 16.5 +/- 6.2 ng/gm WT, whereas in sham injury the y were 1.7 +/- 0.1 ng/gm WT, p less than or equal to 0.005; in the lun g IL-1 alpha levels with cutaneous burn injury were 10.3 +/- 1.3 ng/gm WT, whereas sham injury levels were 1.9 +/- 0.8 ng/gm WT, p less than or equal to 0.002). Levels in all other organs and plasma were below detection limits. Muscle burn injury had similar elevated levels of IL -1 alpha in the liver at 1 hour, indistinguishable from cutaneous burn . In contrast, endotoxin challenge resulted in dramatic elevation of I L-1 alpha levels in all organs tested except for the kidney, whereas t he skin maintained its usual large amounts of IL-1 alpha. Conclusions. These data indicate that thermal or mechanical injury induce very ear ly and organ-specific association of IL-1 alpha in vivo by mechanisms other than endotoxemia.