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Biomedical subjects

H S Jensen

Publications and source records attributed to H S Jensen.

10 recordsLinked to original sources
PubMed1991

Elastolytic activity of human monocytes from synovial fluid and blood of patients with arthritis. Relations to levels of interleukin 6 and soluble interleukin 2 receptor.

Synovial fluid (SF) and blood from 24 patients with non-traumatic, sterile hydarthron were examined for monocyte elastolysis (MøE) and for levels of interleukin 6 (IL-6) and of soluble interleukin 2 receptor (sIL-2R). Six patients had osteoarthrosis (OA) and 18 patients had inflammatory hydarthron (IH), 10 of whom had rheumatoid arthritis (RA). Blood MøE was lower in OA than in IH, both measured as basal MøE activity and after in vitro stimulation with immune complexes and phorbol myristate acetate (PMA). SF MøE was higher than MøE in blood (p less than 0.01). This increase in SF MøE could be mimicked in vitro by prestimulation of blood Mø with low levels of IC. SF IL-6 and sIL-2R were also elevated (p less than 0.01). All three parameters correlated to the degree of joint inflammation evaluated by SF leucocyte level, complement activation, blood C Reactive Protein, and to the clinical evaluation of the joint. The increase in SF MøE, IL-6 and sIL-2R in patients with IH, points to a stimulation of Mø and lymphocytes in the joint.

Adult↗
PubMed1990

Basal and stimulated elastolytic activity of blood monocytes is increased in glucocorticoid-treated giant cell arteritis.

The elastolytic capacity of live human blood monocytes was studied in patients with giant cell arteritis (GA) and in age-matched controls. Despite normalized acute-phase reactants during glucocorticoid (GC) therapy, the basic activity of monocytes from patients with newly diagnosed GA was elevated compared with controls (80 vs. 39 ng/h, p less than or equal to 0.01). The maximum response was enhanced by stimulation with immune complexes (224 vs. 125 ng/h, p less than or equal to 0.01) and with phorbol myristic acetate (324 vs. 214 ng/h, p less than or equal to 0.01). No age difference was found between healthy young and old people. Cell surface related human monocyte elastolytic activity could act as a sensitive marker of cell activation in vivo.

Adult↗
PubMed1989

Blood monocyte elastolytic activity enhanced by immune complex stimulation in patients with rheumatoid arthritis and normal controls. Effect of aurothiomalate or D-penicillamine.

Blood monocyte elastolytic activity in patients with rheumatoid arthritis and in normal controls was studied by a new in vitro technique. The enzyme activity of live cells was measured by soluble [3H]elastin hydrolysis first under basic conditions and then after immune complex stimulation. The cells from patients had a higher elastolytic potential than cells from controls (p less than 0.02) and responded to smaller amounts of immune complex (p less than 0.01), even in patients treated with D-penicillamine or aurothiomalate. Treatment of normal monocytes in vitro with aurothiomalate did not influence the elastolytic response. These findings indicate that monocytes from patients with rheumatoid arthritis have an enhanced elastolytic activity compared with cells from normal controls and may invoke greater tissue damage on immune complex stimulation.

Adult↗
PubMed1987

Prevention of tissue damage: inhibition of myeloperoxidase mediated inactivation of alpha 1-proteinase inhibitor by N-acetyl cysteine, glutathione, and methionine.

The ability of the sulphur compounds, N-acetyl cysteine, Methionine, and Glutathione to prevent inactivation of alpha 1-proteinase inhibitor by Myeloperoxidase-H2O2-Cl--system was investigated in vitro with purified components. The Myeloperoxidase system, or its main product HOCl by itself, readily abrogated the ability of alpha 1-proteinase inhibitor to inhibit elastase. This inactivation of alpha 1-proteinase inhibitor was effectively prevented by micromolar concentrations of N-acetyl cysteine, Methionine and reduced Glutathione, whereas oxidized Glutathione was much less effective. These results indicate that the sulphydryl compounds work as scavengers of the products of the Myeloperoxidase system, and might be useful in inflammatory disorders, to prevent tissue damage inflicted by this system.

Acetylcysteine↗
PubMedDate not supplied

Elastolytic activity of human monocytes: rheumatological aspects.

Activation of human monocytes in rheumatic disorders includes the production of substances active in immunologic interactions, inflammatory responses, and tissue remodelling. This review discusses the cell surface-related elastolytic activity of live human monocytes, as determined by a newly developed elastin assay. Elastase activity was not found to be depressed by patient treatment with glucocorticoids or slow-acting disease modifying drugs nor enhanced by phagocytosis, but was increased by immune complexes in vitro and in patients with rheumatoid arthritis or giant cell arteritis. The leucocyte elastase content seems to be influenced by systemic factors before the monocytes are released into the blood. The enzyme expression of elastase is determined by local factors acting after the cells have left the circulation. Monocyte expression may therefore be a link between immune activation and proteolytic activity.

Animals↗
PubMedDate not supplied

Elastolytic activity of human blood monocytes characterized by a new monoclonal antibody against human leucocyte elastase. Relationship to rheumatoid arthritis.

The leucocyte elastase of human blood monocytes was investigated by applying a new monoclonal antibody which did not block the enzyme activity against elastin. In a fixed population of mononuclear cells (MNC) and using fluorescence activated cell sorting (FACS), the human leucocyte elastase (HLE) antibody identified a subgroup of CD14+ cells which contained all the elastase activity and which could be blocked by a specific chloromethylketone elastase inhibitor. By anti-CD14 labelling the HLE positive cells were identified as monocytes and amounted to 88% of this cell type (median: range 72-96%). In a parallel study of patients with active rheumatoid arthritis (RA) and control donors the elastolytic capacity of PMA-stimulated live MNC was higher for RA patients than for controls (p less than 0.02). For control donors the number of HLE+ cells correlated well to the elastolysis in the same MNC sample (Spearman's rho:0.83, p less than 0.05); in the samples from RA patients no correlation was found between the normal number of HLE+ cells and the increased elastolysis (rho: 0.54, p greater than 0.20).

Adult↗
PubMedDate not supplied

Human monocyte elastolytic activity, the propeptides of types I and III procollagen, proteoglycans, and interleukin-6 in synovial fluid from patients with arthritis.

Elastolytic activity by live human monocytes (M phi) is mainly caused by cell surface related leucocyte elastase, capable of degrading matrix components. In order to examine the possible correlation between enzyme activity and tissue turnover in the joint, we examined 24 synovial fluids for M phi elastolytic activity, using the levels of synovial fluid interleukin-6 and serum C reactive protein as additional markers of cell activation. Proteoglycan levels were measured as an indication of cartilage degradation and the types I and III procollagen propeptides as markers of synovial membrane turnover. We found that elastolysis by live M phi and the levels of interleukin-6 and C reactive protein correlated significantly with proteoglycan concentrations but not with the procollagen propeptides. These findings suggest that human M phi elastolytic activation is a biologically relevant factor in cartilage degradation, but is unrelated to the collagen metabolism of the synovial membrane.

Adult↗
PubMedDate not supplied

Release of elastolytic activity from human monocytes and granulocytes in vitro by immune complex stimulation.

Elastase from phagocytes are neutral proteolytic enzymes and potent destructors of elastic fibres, proteoglycan and collagen. Using soluble 3H-elastin as substrate in a cell culture assay we examined the ability of live, adherent human blood neutrophils and monocytes to release elastolytic activity following immune complex (IC) stimulation. While monocytes increased their elastolysis 2 1/2 times in response to IC (p less than 0.01), neutrophils did not but released lactoferrin and produced superoxide. Both cell types could be stimulated by phorbol myristate acetate (PMA) to increase elastolysis (p less than 0.02) and produce superoxide. Thus, when in contact with the elastin substrate, the in vitro response of monocytes and neutrophils to IC differed with respect to elastolytic release. These findings might be of interest in the understanding of cartilage destruction in immunocomplex-mediated diseases such as rheumatoid arthritis.

Antigen-Antibody Complex↗