Induction of histidine and ornithine decarboxylase activities in mouse tissues by recombinant interleukin-1 and tumor necrosis factor.

The injection of recombinant interleukin-1 (IL-1) into mice induced histidine decarboxylase (HDC) activity in the bone marrow, spleen, lung and liver and ornithine decarboxylase (ODC) activity in the spleen and liver. The ability of IL-1 to induce these responses was the most potent of the various cytokines tested. The induction of these responses by IL-1 seemed to be more rapid than that produced by a lipopolysaccharide. The potency of IL-1 alpha to induce both HDC and ODC activities was similar to that of IL-1 beta, and their combination did not potentiate the induction of these responses. In contrast, although the ability of recombinant tumor necrosis factor-alpha (TNF alpha) to induce these responses was less potent than that of IL-1 alpha or IL-1 beta, the combination of TNF alpha and IL-1 beta produced higher HDC and ODC activities in some tissues tested than those induced by the combination of IL-1 alpha and IL-1 beta. These results suggest that the syntheses of histamine and putrescine are regulated by IL-1 and/or TNF alpha in inflammatory or immune responses. Through these experiments, it was noticed that, in spite of a marked induction of HDC activity in the bone marrow, there was no detectable induction of ODC activity in this tissue. The meaning of HDC induction in the bone marrow is discussed.