Medicine (RMH) - Research Publications
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ItemNo Preview AvailableMacrophage stimulation and the inflammatory response to asbestos.(Environmental Health Perspectives, 1980-02)Chrysotile fibers injected into the peritoneal cavity of mice elicit a cellular exudate. Macrophages appearing in this exudate produce high levels of the neutral protease, plasminogen activator, when compared with the resident peritoneal macrophage population. In contrast, the levels of lysozyme and two lysosomal enzymes are the same for the two macrophage types. The asbestos-induced macrophages producing the plasminogen activator appear to have descended from recently divided precursors. Low concentrations of anti-inflammatory glucocorticoids inhibit macrophage plasminogen activator synthesis. Preliminary experiments indicate that different asbestos types induce hyperemia in skin, and also shorten the partial thromboplastin time of plasma and generate the release of kinins. These observations could be interrelated and are suggested as representing some aspects of the inflammatory response of the host to asbestos exposure.
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ItemNo Preview AvailableSuppression of the neutral protease activity of macrophages treated with asbestos in vitro.(Environmental Health Perspectives, 1983-09)Macrophages are often conspicuous in asbestos-induced inflammatory lesions. Chrysotile type B elicits macrophages into the peritoneal cavity of mice which produce high levels of the neutral protease, plasminogen activator; in vitro addition of these same fibers to mouse peritoneal macrophages stimulates enzyme production. It is reported here that, for endotoxin-elicited mouse peritoneal macrophages fed chrysotile type B in vitro, the increased plasminogen activator activity is suppressed by low concentrations of anti-inflammatory steroids. Other active drugs include colchicine and vinblastine. These studies are considered important, as they suggest an approach to controlling the levels of a potentially deleterious enzyme system (PA-plasmin) from macrophages treated with asbestos fibers.
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ItemNo Preview AvailableAsbestos fibers, plasma and inflammation.(Environmental Health Perspectives, 1983-09)Fibrin clots have been detected at sites of inflammation, and kinins have been implicated as mediators of the vascular phenomena of acute inflammation, systemic shock, and disseminated intravascular coagulation. It is now reported that both negatively and positively charged asbestos fibers shorten the partial thromboplastin time of human plasma, indicating coagulation of the plasma. A sample containing short (less than 5 micron in length) chrysotile fibers is ineffective. Only the negatively charged amphiboles (crocidolite and amosite) are able to activate factor XII (Hageman factor). This particular effect of the amphiboles is enhanced by high molecular weight kininogen and leads to kinin formation.
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ItemHUMAN-MONOCYTES CAN PRODUCE TISSUE-TYPE PLASMINOGEN-ACTIVATOR(ROCKEFELLER UNIV PRESS, 1989-04-01)Evidence has previously been presented that monocytes and macrophages produce urokinase-type plasminogen activator. We have shown for the first time that human monocytes, when stimulated appropriately in vitro, can produce tissue type-plasminogen activator (t-PA) of 70 kD. Detection of t-PA mRNA was consistent with the biochemical and immunological characterization of t-PA produced by human monocytes.
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ItemSTREPTOCOCCAL CELL-WALLS AND SYNOVIAL CELL ACTIVATION - STIMULATION OF SYNOVIAL FIBROBLAST PLASMINOGEN-ACTIVATOR ACTIVITY BY MONOCYTES TREATED WITH GROUP-A STREPTOCOCCAL CELL-WALL SONICATES AND MURAMYL DIPEPTIDE(ROCKEFELLER UNIV PRESS, 1982)Group A streptococcal peptidoglycan has previously been shown to be arthritogenic in rats and has been implicated as a structure present in a class of possible etiologic agents for rheumatoid arthritis. The present study reports that conditioned medium from human monocytes, after interaction with cell wall sonicates of four group A streptococcal strains, stimulates the plasminogen activator (PA) activity of nonrheumatoid synovial fibroblasts. Low concentrations of N-acetylmuramyl-L-alanyl-D isoglutamine (muramyl dipeptide) can also generate this synovial activator (SA) activity from human monocytes. Preliminary biochemical data suggest that the SA activity is distinct from interferon-gamma, interleukin 1, and interleukin 2. These results indicate that agents that are arthritogenic in rats can modulate human synovial fibroblast functions via monocytes. The findings are proposed to have possible significance for an understanding of the cellular interactions involved in the formation and function of the rheumatoid pannus, because PA has been invoked as possibly being generally important for the processes of cell migration, tissue remodeling, and inflammation.
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ItemMACROPHAGE TUMOR-CELL LINE AND PLASMINOGEN ACTIVATOR - POTENTIAL MODEL SYSTEM FOR MACROPHAGE REGULATION OF ENZYME-PRODUCTION(ROCKEFELLER UNIV PRESS, 1978)The macrophage cell line, RAW264.10, synthesizes and secretes plasminogen activator. Production of this enzyme is inhibited by low concentrations of glucocorticoids and increased by phorbol myristate acetate. It is proposed that this line could be a suitable model for the regulation of enzyme synthesis by mouse peritoneal macrophages.
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ItemMACROPHAGE PLASMINOGEN ACTIVATOR - INDUCTION BY ASBESTOS IS BLOCKED BY ANTI-INFLAMMATORY STEROIDS(ROCKEFELLER UNIV PRESS, 1976)Intraperitoneal injection of asbestos fibres into mice induces the formation of exudates containing macrophages that produce plasminogen activator. Like-wise, in vitro addition of asbestos to macrophage cultures stimulates plasminogen activator secretion; the synthesis and secretion of lysozyme and lysosomal enzymes are not changed under these conditions. The enhanced secretion of plasminogen activator by macrophages exposed to asbestos is suppressed by low concentrations of anti-inflammatory steroids.
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ItemCell-to-cell interaction in the immune response. VII. Requirement for differentiation of thymus-derived cells.(Rockefeller University Press, 1971-11-01)Experiments were designed to test the possibility that thymus-derived (T) cells cooperate with nonthymus derived (B) cells in antibody responses by acting as passive carriers of antigen. Thoracic duct lymphocytes (TDL) from fowl gammaG-tolerant mice were incubated in vitro with fowl anti-mouse lymphocyte globulin (FALG), which was shown not to be immunosuppressive in mice. On transfer into adult thymectomized, irradiated, and marrow protected (TxBM) hosts together with a control antigen, horse RBC, a response to horse RBC but not to fowl gammaG was obtained. By contrast, TxBM recipients of nontolerant, FALG-coated TDL responded to both antigens and the antibody-forming cells were shown to be derived from the host, not from the injected TDL. These findings suggested that, under the conditions of the experiment, triggering of unprimed B cells in the spleens of TxBM hosts was not achieved with antigen-coated tolerant lymphocytes. Another model utilized the ability of B cells to bind antibody-antigen complexes. Spleen cells from TxBM mice, incubated in vitro with anti-fowl gammaG-fowl gammaG.NIP, were injected with or without normal TDL (a source of T cells) into irradiated hosts. Only mice given both cell types could produce an anti-NIP antibody response. In a further experiment, spleen cells from HGG.NIP-primed mice were injected together with NIP-coated B cells (prepared as above) into irradiated hosts. A substantial anti-NIP antibody response occurred. If, however, the T cells in the spleens of HGG.NIP-primed mice were eliminated by treatment with anti-theta serum and complement, the NIP response was abolished. It was concluded that antigen-coated B cells could not substitute for T cells either in the primary or secondary response. Treatment of T cells from unprimed or primed mice with mitomycin C impaired their capacity to collaborate with B cells on transfer into irradiated hosts. Taken together these findings suggest that before collaboration can take place T cells must be activated by antigen to differentiate and in so doing may produce some factor essential for triggering of B cells.