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C K Abrass

Publications and source records attributed to C K Abrass.

51 records · Page 3Linked to original sources
PubMed1985

Characterization of the beta-adrenergic receptor of the rat peritoneal macrophage.

The beta-adrenergic receptor was characterized on BCG-activated rat peritoneal macrophage membranes by radio-ligand binding studies. Saturable binding with [125I]iodocyanopindolol (125I-ICYP) was demonstrated. With Scatchard analysis, rat macrophages demonstrate approximately 1000 receptors per cell with a Kd of 5 X 10(-11) M for 125I-ICYP. Competition curves with (-) and (+) propranolol at concentrations below 10(-6) M confirmed stereospecificity. The potency of various ligands to compete for 125I-ICYP binding sites followed the order: propranolol greater than isoproterenol greater than epinephrine greater than norepinephrine with apparent Kd of 2.0 X 10(-9), 3.9 X 10(-7), 1.0 X 10(-5), and 2.5 X 10(-5) M, respectively. Isoproterenol-stimulated adenylate cyclase activity was two-fold above basal activity. The potential physiologic significance of a beta-adrenergic receptor on rat peritoneal macrophages was suggested by a dose-dependent decrease in phagocytosis of soluble, model immune complexes (aggregated gamma-globulin) by macrophages incubated with metaproterenol. We conclude that the rat macrophage has a beta-adrenergic receptor and that catecholamines may thereby modulate macrophage function.

1-Methyl-3-isobutylxanthine↗
PubMed1984

Therapeutic percutaneous renal artery occlusion with a detachable balloon.

Bilateral nephrectomy is sometimes required for the control of severe hypertension or nephrotic syndrome. Surgical intervention in a patient with uncontrollable hypertension or the malnutrition and anasarca of nephrotic syndrome is associated with increased risk for the development of operative complications. We report 2 hemodialysis patients, 1 with uncontrollable hypertension and 1 with nephrotic syndrome, who were successfully treated with percutaneous renal infarction. Inflatable and detachable balloons were placed in each renal artery by percutaneous arterial catheterization. Neither patient experienced any significant complication from the procedure.

Adult↗
PubMed1984

Alterations in Fc receptor function of macrophages from streptozotocin-induced diabetic rats.

The presence of elevated levels of circulating immune complexes in diabetic humans and animals suggests impaired phagocyte function. To evaluate FcR-mediated phagocytosis, resident peritoneal macrophages were harvested from control, streptozotocin-induced diabetic, and insulin-treated diabetic rats. FcR number and avidity were determined from Scatchard analysis of binding of 125I-labeled aggregated rat IgG (ARG) to macrophages. The total and fractional catabolic capacity were determined by quantitating the digestion of ARG as a percent of the total ARG added and as a percent of ARG bound. Insulin-deficient diabetic rats had an increase in the number of FcR per cell (26.8 +/- 3.5 X 10(4)) as compared with control animals (13.1 +/- 1.2 X 10(4)) (p less than 0.01). In contrast, insulin-treated diabetic animals had a reduction in the number of FcR per cell (9.8 +/- 1.4 X 10(4)) (p less than 0.01). FcR of macrophages from insulin-deficient diabetic rats had a lower avidity (Kd = 6.9 +/- 1.8 X 10(-10)M) when compared with control (3.7 +/- 0.6 X 10(-10)M) and insulin-treated diabetic rats (3.6 +/- 0.9 X 10(-10)M) (p less than 0.01). Total catabolism of ARG by macrophages from both insulin-deficient and insulin-treated diabetic rats was reduced (31.0% +/- 3.4 and 17.5% +/- 3, respectively) when compared with controls (49.6% +/- 5.2) (p less than 0.01). Fractional catabolism by macrophages from insulin-deficient diabetic rats was significantly reduced (21% +/- 1.9 and 4.6% +/- 0.9/10(4) FcR) when compared with results from control rats (26% +/- 1.3 and 6.7% +/- 0.7/10(4) FcR) (p less than 0.01), whereas the results from insulin-treated diabetic rats (32% +/- 2.4 and 10.8% +/- 1.0/10(4) FcR) (p less than 0.01) were greater than those from controls. These studies demonstrate that FcR-mediated phagocytosis of soluble, "model" immune complexes is impaired in macrophages from both insulin-deficient and insulin-treated diabetic rats; however, different mechanisms account for this impairment in phagocytosis. Despite an increase in FcR number of macrophages from insulin-deficient diabetic rats, the depression of post-receptor-mediated catabolism results in a net depression in phagocytic activity. In contrast, macrophages from insulin-treated diabetic rats display augmented post-receptor-mediated catabolism; however, this does not overcome the low initial binding of ARG to the cell that results from the depression of FcR number.

Animals↗
PubMed1984

Evaluation of the presence of circulating immune complexes and their relationship to glomerular IgG deposits in streptozotocin-induced diabetic rats.

Circulating immune complexes (CIC) have been postulated to contribute to the development of secondary complications in diabetes mellitus. In this study, CIC were measured in control rats and both insulin deficient and insulin treated streptozotocin-induced diabetic rats. CIC were more prevalent in both groups of diabetic rats as determined by the fluid and solid phase Clq binding assays. By 42 days after induction of diabetes, 80% of insulin deficient and 50% of insulin treated rats had detectable CIC by either/or both assays. As determined by direct immunofluorescence, there was progressive accumulation of rat IgG in the glomerular mesangium. The presence of CIC paralleled the glomerular deposition of IgG. The relationship of circulating insulin levels to the clearance of CIC and the glomerular deposition of IgG is discussed.

Animals↗
PubMed1984

Autologous immune complex nephritis in rats. Influence of modification of mononuclear phagocyte system function.

These studies were designed to determine the effect of modification of mononuclear phagocyte system function on a chronic immune complex disease. Autologous immune complex nephritis in rats (Heymann nephritis) was induced by immunization with renal tubular epithelial antigen (Fx1A). The mononuclear phagocyte system was impaired by splenectomy and stimulated by weekly intraperitoneal injections of zymosan. Serial determinations included 24-hour urinary protein excretion, serum antibody titers, C3, circulating immune complexes, creatinine, and creatinine clearance. Renal tissue was obtained at 21, 42, and 56 days after immunization to evaluate by immunofluorescence the amount of antigen and IgG deposited. Splenectomized rats with Heymann nephritis had significantly greater amounts of glomerular Fx1A antigen and IgG deposits at each time studied than did rats without modification of mononuclear phagocyte system function. Zymosan-treated rats had very few glomerular deposits. In the splenectomized rats, the creatinine clearance was depressed by 50%. All animals had normal levels of C3 and identical antibody titers. In an independent assessment of mononuclear phagocyte system function, plasma clearance of Fx1A was enhanced in zymosan-treated animals and depressed in splenectomized animals. These modifications of mononuclear phagocyte system function were associated with changes in the amount of glomerular deposits of IgG and the clinical course of membranous nephropathy in this animal model. Application of methods for stimulation of mononuclear phagocyte system function may have therapeutic efficacy in the future treatment of human membranous nephropathy.

Animals↗
PubMed1983

Impaired response of neutrophils to a lymphokine by sera from patients with connective tissue disease.

The studies reported here were designed to determine whether sera from various patients could prevent neutrophils from responding to the lymphokine, neutrophil migration inhibition factor from T lymphocytes (NIF-T). Neutrophils from healthy donors were treated with sera from 84 subjects and assayed for responses to NIF-T. Serum from 7 of 37 patients (19%) with rheumatoid arthritis, systemic lupus erythematosus, and various forms of vasculitis showed blocking activity. In contrast, none of 47 subjects, including healthy individuals and patients with spondylarthropathies, cancer, and active infections had a serum factor that prevented neutrophils from responding to NIF-T (P less than 0.01). Serum blocking activity occurred transiently in association with infection by Staphylococcus aureus in one patient with rheumatoid arthritis. Moreover, autologous neutrophils from this same patient showed impaired responses to NIF-T. Blocking activity could be eluted from protein A-Sepharose in three of three patients studied. In three of seven patients, blocking activity was detected in serum cryoprecipitates, with a recovery of 46 to 78% of the blocking activity and overall enrichment (purification) of 137- to 281-fold. Analysis of cryoprecipitates by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed the predominance of immunoglobulins M and G. In one patient, the serum blocking activity was not cryoprecipitable, and cryoprecipitates from a patient with essential cryoglobulinemia failed to prevent neutrophils from responding to NIF-T. Blocking activity was relatively specific for NIF-T, as there was no effect on F-met-leu-phe-induced chemotaxis of neutrophils. Serum blocking activity in patients with connective tissue disease showed some correlation (r = 0.50; P less than 0.01) with immune complexes detected by polyethylene glycol precipitation but not Clq binding. These studies suggest that the response of neutrophils to NIF-T may be blocked by serum, possibly as a result of immune complexes or autoantibodies found primarily in patients with connective tissue disease.

Antigen-Antibody Complex↗
PubMed1983

Circulating immune complexes in patients with diabetes mellitus.

Circulating immune complexes (CIC) were detected by the solid phase C1q binding assay in 16% of 103 diabetic patients and by the fluid phase C1q binding assay in 31% of patients as compared to 5% of 58 control subjects for each assay. Plasma glucose determinations revealed that most patients were moderately hyperglycaemic (mean glucose = 264 mg/dl), and thus were not selected for tight metabolic control. All but six patients had elevated levels of plasma insulin, including both the insulin treated and diet treated subgroups. There was no correlation between the presence of CIC detected by either assay and plasma glucose, insulin, or the presence of microangiopathy. Multiple factors must contribute to the increase in CIC in both insulin deficient and insulin resistant diabetics. The role of these various factors remains to be defined.

Adult↗
PubMed1980

Correlation and predictive accuracy of circulating immune complexes with disease activity in patients with systemic lupus erythematosus.

Serial serum samples from 48 patients with systemic lupus erythematosus (SLE) were assayed for C3, anti-DNA antibody, and circulating immune complexes (CIC). CIC were measured by the fluid phase (FClq) and solid phase (SClq) Clq binding assays. Elevations of the SClq results were associated with the presence of manifestations of SLE (P less than 0.001), including active renal disease (P less than 0.005) and arthritis (P less than 0.001), as well as changes in degree of disease activity which prompted physician action. A change in the SClq results correctly predicted a change in disease activity 82% of the time (P less than 0.005). Abnormalities of FClq, anti-DNA antibody, and C3 were neither associated with nor predictive of changes in disease activity of SLE. These data suggest that the SClq method of determining CIC is the most reliable laboratory indicator of clinical activity in SLE.

Adolescent↗
PubMed1980

Circulating immune complexes in rats with autologous immune complex nephritis.

Autologous immune complex nephritis (Heymann nephritis) was actively induced in rats by immunization with high (10 mg.) and low (1 mg.) doses of renal tubular epithelial antigen in complete Freund's adjuvant. The development of proteinuria and granular capillary wall deposition of IgG confirmed the previously well described membranous nephropathy which characterizes this experimental disease. Circulating immune complexes were demonstrated by both the fluid phase and solid phase C1q binding assays in both high and low dose experimental groups. The prevalence of such immune complexes was significantly greater in the experimental than in the control groups immunized with adjuvant alone or liver homogenate in adjuvant. The circulating immune complexes bound to C1q were 16 to 23 S in size and were proven to contain a renal tubular antigen. These data, in combination with the previous demonstration of renal tubular antigen and its antibody in kidneys from rats with autologous immune complex nephritis, are consistent with a circulating immune complex pathogenesis of this model of the actively induced autologous immune complex nephritis in rats.

Animals↗
PubMed1980

Non-specificity of circulating immune complexes in patients with acute and chronic liver disease.

Circulating immune complexes have been described in viral hepatitis and primary biliary cirrhosis but their significance is unclear. Seventy-three patients with acute and chronic liver diseases were evaluated to determine the specificity of immune complex detection for a given liver disease. Immune complexes were measured by the fluid- and solid-phase Clq-binding assays. They were demonstrated frequently in all patients with liver disease, including those with viral hepatitis, alcoholic cirrhosis, chronic active and persistent hepatitis, drug-induced hepatitis and hepatic metastases. The presence of immune complexes was not specific for a given type of liver disease and did not correlate with hepatic dysfunction. We conclude that the detection of immune complexes is of no apparent diagnostic use in liver disease. Further evaluation of the antigen-antibody composition would be required to determine any pathogenic significance of the detected circulating immune complexes.

Acute Disease↗
PubMedDate not supplied

Role of laminin isoforms in glomerular structure.

Laminin along with collagen type IV, proteoglycans, and entactin are major components of basement membranes. Basement membrane components are synthesized at high levels during development. The formation of specialized basement membranes may play important roles in cell and tissue function by influencing cell proliferation, phenotype, migration and gene expression as well as tissue architecture. The growing diversity of laminin isoforms influences the formation of distinct basement membranes. Many of the laminin chains sequenced to date are expressed during glomerular development under strict temporal control. Also, some studies suggest that additional laminin chains exist and contribute to unique isoforms expressed within the renal glomerulus. This article will review the status of characterization of laminin isoforms expressed by glomerular cells, point out possible differences in isoforms expressed by different species, and discuss the implications of the complexity of glomerular laminins. In order to fully understand the nature of the glomerular laminins and their importance, information from studies of cells in culture, whole tissue, and those that use molecular and protein analysis must be integrated.

Animals↗