PubMed · 1981 · 23 citations · 13 references
Life SciencesImmunologyPathologyImmunopathologyInflammationInnate ImmunityCartilage MetabolismCytokine BiologyCytokine RegulationInflammatory MediatorsMacrophage BiologyArticular Cartilage LossCartilage Breakdown PathophysiologyCartilage DestructionCartilage Protease ActivityExtracellular ProteasesImmunomodulation In Cartilage RegenerationInflammatory Mediators In CartilagePeritoneal Macrophages
Cultured rabbit peritoneal macrophages, after stimulation with lipopolysaccharides (LPS), produce a factor that induces normal rabbit articular cartilage cells (chondrocytes) to release collagenase and other neutral proteases in their culture medium. The release of the factor as well as the activation of chondrocytes can be significantly inhibited by paramethasone (10(-6) M). Rabbit peripheral blood monocytes produce this factor in smaller quantities. Activation with LPS does not enhance the release of factor any further by these cells. Lymphocytes have no direct effect on the chondrocytic protease synthesis. Furthermore, conditioned medium of activated lymphocytes failed to stimulate monocytes or macrophages in the absence of LPS. The macrophage medium exhibits mitogenic and phytohaemagglutinin-enhancing activity towards thymocytes of C3H/HeJ mice, but not against species-specific rabbit lymphocytes. The lymphocyte-activating factor, derived from a mouse macrophage cell line, P388D1 cells, or from other sources, was unable to stimulate chondrocytic protease secretion. Such specific induction of chondrocytic proteases by a macrophage-derived factor may have an important role in cartilage destruction in arthritic conditions, where synovium is only marginally involved.
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J H Korn, Perry V. Halushka, E. Carwile LeRoy · Journal of Clinical Investigation · 1980 · 282 citations · Full text
Jean‐Michel Dayer, J Bréard, Leonard Chess et al. · Journal of Clinical Investigation · 1979 · 281 citations · Full text