In vivo expression of interleukin-1 receptors during various experimentally induced inflammatory conditions.

Systemically administered interleukin-1 (IL-1) has been shown to preferentially bind to IL-1 receptors (IL-1Rs) in inflammation. Using radiolabeled IL-1alpha and molecular methods to assess gene expression for these receptors, the in vivo behavior of these receptors was investigated in a number of experimental inflammatory conditions. The uptake of 125I-labeled IL-1alpha in inflammatory foci significantly correlated with the mRNA expression for the type I and type II IL-1Rs (P < .05). Type II IL-1R mRNA showed a greater increase in expression than type I IL-1R mRNA. In neutropenic mice, inflammatory lesions, which are devoid of granulocytes, significantly lower 125I-labeled IL-1alpha uptake (P < .001), and type II IL-1R mRNA expression (P < .005) was found. Thus, there is strong up-regulation of IL-1Rs at sites of focal inflammation. Of interest, this mainly involved the type II IL-1R on granulocytes, which is not involved in signal transduction.