Studies designed to characterize monocyte-derived recruiting activity (MRA) a monokine that stimulates endothelial cells to produce granulocyte macrophage-colony-stimulating activity (CSA) by endothelial cells, show that it is a thermolabile protein of from 12,000 to 24,000 D which, on chromatofocusing, shows three separate peaks of eluted activity from pH 7.5 to 5.0. Because these and many other properties of MRA are identical to those of interleukin 1 (IILi), we tested the hypothesis that MRA and IL-I are identical. We cultured vascular endothelial cells with various concentrations of purified native and recombinant IL-i (pI 7 form), then tested the endothelial cell supernatants for GM-CSA. Purified native IL-i and recombinant IL-i stimulated endothelial cells to release CSA. The MRA of native IL-1, recombinant IIL-, and unfractionated monocyte conditioned medium was neutralized by a highly specific rabbit anti-human IL-1 antiserum. Chromatofocusing fractions that contained MRA contained immunoreactive IL-1 on immunoblotting and the bioactivity was neutralized completely by treatment with the antiserum. We conclude that IL-i induces the release of CSA by vascular endothelial cells, that IL-1 is constitutively produced by monocytes in vitro, and that MRA and IL-i are biologically, biophysically and, immunologically identical.
The histopathologic changes reported here in the C3H/HeJ mouse model of chronic otitis media have been reported in human chronic otitis media. This spontaneous model of chronic otitis media will be valuable for the characterization of middle and inner ear inflammatory disease processes that are induced by middle ear infections.
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