[Sclersong peritonitis during practolol (Eraldine) therapy].
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Aged↗
Biomedical subjects
K Bendtzen
Publications and source records attributed to K Bendtzen.
An in vitro assay of leukocyte migration inhibitory activity from human lymphocytes stimulated with concanavalin A.
Human venous blood lymphocytes, incubated for 22 h in serum-free culture medium with the plant mitogen concanavalin A (Con-A), elaborated products, which inhibited the migration of human buffy coat cells under agarose. Con-A was removed by applying the supernatants on small Sephadex G-100 columns. The leukocyte migration inhibitory activity (LMIA) was tested in a semi-quantitative modification of the indirect leukocyte migration agarose technique, which is described. Lymphokine activity, demonstrable as early as 9 h after activation of lymphocytes, was most pronounced after 22 h. Significant LMIA was demonstrated in 12 of 17 normal individuals at standard dilution of culture supernatants I/3. In 9 of the 12 experiments, assays of LMIA were carried out on stepwise diluted supernatants with detection of the greatest dilution with significant LMIA. In four experiments LMIA could only be detected after 3- to 12-fold concentrations of supernatants. Considerable individual variation was found, the amounts of LMIA varying by a factor of about 300. The reproducibility appeared to be quite high, but the factor stability of supernatants stored at -20 degrees C was surprisingly low.
Adult↗
Inhibition of human leukocyte migration inhibitory factor (LIF) by alpha-L-fucose.
Peak leukocyte migration inhibitory activity was produced in vitro by human lymphocytes stimulated with concanavalin A and eluted from Sephadex G-100 gel columns in fractions containing molecules of mol. wt. 40,000-50,000 daltons. No activity was found in fractions containing molecules of mol. wt. 23,000 daltons which is the estimated size of the human macrophage migration inhibitory factor (MIF). In the present experiments migration inhibition was tested on human peripheral blood leukocytes migrating under agarose. Unconcentrated supernatant activity was reduced in a dose-related manner by alpha-L-fucose. At a concentration of 0.1 M alpha-L-fucose, the mediator activity was completely neutralized. The effect was reversible and specific for alpha-L-fucose. Concentrated supernatant activity, however, was only slightly reduced even in the presence of a higher concentration of sugar. The possible role of alpha-L-fucose as a part of a mediator receptor on the indicator cells is discussed.
Adult↗
[Ampicillin induced bacteriuria in children].
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Adolescent↗
The role of monocytes and T cells in 1,25-dihydroxyvitamin D3 mediated inhibition of B cell function in vitro.
1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) inhibits immunoglobulin production by human mononuclear cells (MNC) in vitro. The present study was undertaken to evaluate the role of T cells and monocytes in 1,25-(OH)2D3 induced suppression of B cell functions. The synthetic vitamin D3 analogue MC 903 was examined in parallel. 1,25-(OH)2D3 and MC 903 showed a dose-related inhibition of IgM, IgG and IgA plaque-forming cells in poke-weed mitogen (PWM) activated cultures of MNC. This effect was most likely mediated through impairment of T cell and monocyte functions. First, the inhibitory effect was seen after PWM stimulation, but not after Epstein-Barr virus stimulation which activates B cells independently of T cells and monocytes. Second, 1,25-(OH)2D3 was not effective in T cell and monocyte-depleted cultures. Third, the effect of 1,25-(OH)2D3 on PWM driven MNC was reversed by addition of the recombinant monokines: interleukin (IL)-1 beta, tumour necrosis factor alpha (rTNF alpha), rIL-6, as well as the lymphokines: lymphotoxin (rLT) and rIL-2. This is consistent with the finding that 1,25-(OH)2D3 also inhibited IL-1 alpha, TNF alpha and LT production in these cultures. The assumption that B cells are not directly affected by 1,25-(OH)2D3 was further supported by the fact that 24 h of culture with 10(-8) M 1,25-(OH)2D3 failed to reduce immunoglobulin production by in vivo activated B cells.
Antibody Formation↗
Eosinophil cationic protein and eosinophil protein X: human amniotic fluid concentrations and gestational tissue content at term.
The aim of this study was to determine the presence and concentration of immunoreactive eosinophil cationic protein (ECP) and eosinophil protein X (EPX) in human amniotic fluid at term and assess labour-associated changes in their mean concentrations. In addition, ECP and EPX content in term amnion, choriodecidua and placenta obtained before and after labour and delivery was established. Immunoreactive ECP and EPX were identified in all samples of amniotic fluid (n=47) and gestational tissue (n=60) assayed. EPX was quantitatively more abundant than ECP in both amniotic fluid and gestational tissues. In amniotic fluid, ECP and EPX concentrations increased 8-fold (P<0.02) and 1.5-fold (P<0.02), respectively, with labour onset. In gestational tissues, a labour-associated change in tissue content was only identified for ECP in choriodecidua, which increased 1.9-fold with labour and delivery (P<0.01). The labour-associated increase in amniotic fluid concentrations of ECP and EPX demonstrated in this study is consistent with the well-characterized role of these proteins in inflammatory reactions. It remains to be established whether the observed increase in ECP and EPX amniotic fluid concentrations is an epiphenomenon of labour onset or is involved causally in this process.
Adult↗
Morphological effects of sodium fusidate (fusidin) on pancreatic islet cells: an electron microscopic study.
Fusidic acid has been shown to prevent the lymphocyte co-stimulatory activities of cytokines and seems--in preliminary trials--clinically effective as an immunoregulatory drug e.g. in insulin-dependent diabetes mellitus. A toxic effect of fusidic acid may however be suspected since a previous study showed a significant dilatation of rough endoplasmic reticulum in cultured pancreatic islet cells from normal rats. In this study we examined the ultrastructural effects of the sodium salt of fusidic acid (fusidin) on cultured rat islet cells (treatment period 3-5 days), and of islet cells from rats receiving fusidin for 6 days. Electron microscopically, fusidin treatment in vitro (3 to 30 micrograms/ml) showed a significant dilatation of the rough endoplasmic reticulum of islet cells. No dose dependent changes were found. In the in vivo model no changes were demonstrated in concentrations of fusidin up to 9.64 micrograms/ml of homogenated pancreatic tissue. It is concluded that treatment with fusidin gives no detectable ultrastructural changes in vivo.
Animals↗
Cytokines (immunoinflammatory hormones) and their natural regulation in inflammatory bowel disease (Crohn's disease and ulcerative colitis): a review.
Cytokines, particularly the proinflammatory cytokines, whose role and natural regulation in inflammatory bowel disease are reviewed here, are produced by many cell types, including immune cells. Cytokines function as important hormones of the immune system, and many act both regionally and systemically via specific receptors. The demonstration of increased circulating and mucosal levels of proinflammatory (and other) cytokines (and receptors) in active inflammatory bowel disease does not by itself constitute any proof as to the primary involvement of these mediators. However, they may contribute significantly to disease manifestations, and specific therapeutic intervention at the cytokine or cytokine receptor level may show up to be clinically most relevant. This is underscored by the increasing evidence that proven therapies of inflammatory bowel disease to a great extent seem to function through cytokine modulation.
Animals↗
Adhesion molecules in inflammatory and neoplastic intestinal diseases.
Adhesion molecules participate in a broad variety of biological processes, i.e. tumor progression and inflammation, through their involvement in cell-to-cell interactions and immunoinflammatory cell migration. This review describes the basic properties of adhesion molecules with reference to inflammatory bowel disease and colorectal carcinoma. Accumulating data suggest that adhesion molecules could be pathogenetically pertinent to other gastrointestinal disorders such as celiac disease (nontropical sprue) and gastroduodenal ulcer. Future therapeutic approaches in inflammatory and malignant disorders may possibly be development of principles targeting adhesion molecules.
Cell Adhesion Molecules↗
Patient-specific cell-mediated immunity against human acoustic neuroma extract.
Lymphocytes from 8 patients with acoustic neuromas and 8 healthy control persons were exposed to acoustic neuroma extract. Indirect leukocyte migration agarose technique was applied for detection of leukocyte migration inhibition (LMI). The standard technique was additionally modified using a specific assay for release of human leukocyte migration inhibitory factor (LIF). Both the standard technique and the LIF-specific assay revealed a significant LMI exerted by lymphocytes from patients, as compared with control persons. The LIF-specific assay demonstrates that the LMI is an expression of cell-mediated immunity due to release of LIF. The immune reaction is raised against an unknown antigen in acoustic neuroma extract. Further studies must determine whether the immune reaction is specific for acoustic neuroma patients vis-a-vis patients with other tumours, especially other neuromas.
Adult↗
Antigenicity and protein content of perilymph in acoustic neuroma patients.
11 acoustic neuroma patients, exhibiting cell-mediated immunity in vitro against acoustic neuroma extract, were tested for cell-mediated immunity in vitro against perilymph samples from other acoustic neuroma patients. 14 of 21 perilymph samples were antigenic. None of three healthy persons reacted against antigenic perilymph samples. The perilymph antigenicity was reproducible and negatively correlated to the perilymph sample volume. Differences in sample volume could not be ascribed to admixture of endolymph, cerebrospinal fluid, plasma or blood. The perilymph protein concentration varied from 31 to 54 g/l. Gel electrophoresis of perilymph proteins revealed less staining in the alpha-region compared to plasma proteins and a distinct band in the pre-gamma region absent in plasma. Tau-transferrin was not detected in any of 13 samples. The findings support that the cell-mediated immune response against acoustic neuroma extract may be mediated through release of antigen(s) to the perilymph.
Adolescent↗
TNF and LT binding capacities in the plasma of arthritis patients: effect of etanercept treatment in juvenile idiopathic arthritis.
BACKGROUND: Etanercept (Enbrel) induces a rapid and sustained decline in disease activity in the majority of patients with refractory juvenile idiopathic arthritis (JIA). For unknown reasons, however, a number of JIA patients fail to respond to this therapy. During this treatment neutralisation of tumour necrosis factor (TNF, previously termed TNF alpha) and lymphotoxin (LT, previously termed TNF beta) may be mediated by etanercept itself as well as by naturally occurring soluble TNF receptors. In light of this, it was of interest to study the total TNF neutralizing capacity in plasma before and during treatment with etanercept. RESULTS: In initial experiments plasma samples from healthy individuals were incubated with etanercept, and spiked with TNF or LT to a final concentration of 1000 pg/mL. Detection of TNF and LT by ELISA was found to be reduced by approximately 50% and 80% respectively, at a concentration of etanercept of 5-500 ng/mL, which is close to the pharmacological plasma concentrations. Plasma samples (n = 80) were then collected from 12 JIA patients (5 with pauciarticular, 5 with polyarticular and 2 with the systemic onset type) during treatment with etanercept (0.4 mg/kg twice weekly) for a period of 20.8 (15.6-23.9) months (median, range). The plasma samples were spiked with LT, and the inhibition of LT detection in ELISA was measured. In samples obtained 3 months after the start of etanercept, the inhibition of LT detection was augmented [72% (60-85)] compared with pre-treatment samples [16% (0.32)] (p = 0.0039). These findings were confirmed in binding assays using radiolabelled TNF. Among patients who responded insufficiently to therapy, reduced LT binding capacity, coinciding with flares of disease activity, was observed. CONCLUSION: We have developed an assay by which LT binding capacity, reflecting the level of free, pharmacologically active etanercept, may be monitored in the blood of patients treated with etanercept. This assay may prove to be useful in guiding dose adjustments in patients with an incomplete response to etanercept.
Adolescent↗
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↗
Interleukin-1 receptor antagonist in neonates, children and adults, and in patients with pauci- and polyarticular onset juvenile chronic arthritis.
OBJECTIVE: The production of interleukin (IL) -1 alpha IL-1 beta and IL-1 receptor antagonist (IL-1ra) by blood mononuclear cells (MNC), as well as the corresponding serum levels of IL-1ra were examined in blood samples from umbilical cords (n = 11), children (n = 40) and adults (n = 20), and in 42 patients with juvenile chronic arthritis (JCA) of the pauci- or polyarticular onset type. RESULTS: IL-1ra serum levels were found to differ significantly between the three age groups, being higher in neonates (569 pg/ml) than in children (70 pg/ml) and adults (177 pg/ml). IL-1ra production in E. coli lipopolysacharide (LPS) stimulated-cultures of MNC was also significantly higher in neonates (median 2451 pg/ml) than in children (1526 pg/ml), but similar to that in adults (2107 pg/ml). IL-1ra levels in the sera of both subgroups of JCA patients were significantly elevated (median 257 pg/ml), but did not reflect paraclinical or clinical disease parameters. In samples of synovial fluid the IL-1ra levels tended to be fairly high, up to approximately 2 ng/ml, but they did not reflect the serum levels of IL-1ra. CONCLUSION: These findings suggests that the upregulation of IL-1ra production forms part of the immunoregulatory response in JCA patients, and that the insufficient production of IL-1ra is unlikely to contribute to the pathogenesis of JCA.
Adolescent↗