The aim of this study was to examine whether interleukin-13 (IL-13), a cytokine with anti-inflammatory activities, affected expression of interleukin-1 (IL-1) receptors (R) in human polymorphonuclear cells (PMN). Treatment with IL-13 augmented both type I and type II (decoy) R transcripts, with the latter being by far the most represented. The transcriptional inhibitor actinomycin D blocked the induction of IL-1 R mRNAs by IL-13. Nuclear run-off experiments demonstrated an augmented transcriptional rate of IL-1 decoy R in IL-13-treated B lymphoblastoid cells. The protein synthesis inhibitor cycloheximide blocked type I R expression but superinduced decoy R expression. IL-13 augmented the binding of radiolabeled IL-1 beta on the PMN surface with an increased number of IL-1 receptors and no change in Kd values. IL-13 induced the surface expression of IL-1 decoy R and the release by PMN of an IL-1-binding protein identified as a soluble version of the IL-1 decoy R. These results show that PMN is an important target for IL-13 and that induction of expression and release of the IL-1 decoy R, in concert with inhibition of cytokine synthesis, may represent an important mechanism by which IL-13 blocks IL-1, a central mediator of inflammatory reactions.