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 cytokine activation in vivo with a sensitive radioimmunoassay specific for rat interleukin-1 alpha (IL-1 alpha).

METHODS

We characterized the organ distribution and expression kinetics of IL-1 alpha in rats submitted to either 20% total body surface area cutaneous burn, muscle burn, 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).

RESULTS

Thermal injury induced marked elevations of IL-1 alpha levels in the liver and lung, and maximal levels were reached at 2.5 hours when compared with controls. In the liver mean IL-1 alpha levels in cutaneous burn injury were 16.5 +/- 6.2 ng/gm WT, whereas in sham injury they were 1.7 +/- 0.1 ng/gm WT, p < or = 0.05; in the lung 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 < or = 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 IL-1 alpha levels in all organs tested except for the kidney, whereas the skin maintained its usual large amounts of IL-1 alpha.

CONCLUSIONS

These data indicate that thermal or mechanical injury induce very early and organ-specific association of IL-1 alpha in vivo by mechanisms other than endotoxemia.