Biomedical subjects

R Zubler

Publications and source records attributed to R Zubler.

4 recordsLinked to original sources

PubMed1979

Complement activation in pneumonia.

Complement analyses performed on serially collected plasma samples from 10 patients during acute infectious pneumonia or bronchopneumonia showed normal or increased values for hemolytic activity and Clq, C4, C3, and factor B levels. However, the levels of C3 breakdown products (C3d) were significantly (greater than 2 SD) increased in six patients during the first three days of observation, suggesting that hypercatabolism of complement components may occur during the acute phase of infectious pneumonia concomitant with a hypersynthesis of some complement components. Evidence of circulating immune complexes was obtained only in two patients with the 125I-Clq Binding Test.

Acute Disease↗

PubMed1979

Decreased heat-labile opsonic activity and complement levels associated with evidence of C3 breakdown products in infected pleural effusions.

Heat-labile opsonic activity was measured simultaneously in serum and pleural fluid of patients with transudates, infectious exudates (with positive or negative bacterial culture) and neoplastic exudates, using two different complement-dependent phagocytic tests: the killing of Staphylococcus aureus Wood 46 variant strain (K50 opsonic titers) and the assessment of ingestion rate of endotoxin-coated paraffin particles (Oil Red 0 uptake test). K50 opsonic titers were lower in culture-positive pleural effusions as compared to culture-negative (P < 0.002) or neoplastic effusions (P < 0.002). These results were corroborated by the Oil Red 0 uptake test. The data obtained with the two assays showed a significant correlation (P < 0.001). The hemolytic activity of complement (CH50) as well as the levels of C3 breakdown product, C3d, were measured in the same sera and pleural fluid samples and in an additional group of patients with pleural effusions of the same etiology. Effusions with positive cultures showed lower CH50 values (P < 0.01) and higher C3d values (P < 0.05) when compared to culture-negative pleural fluids. Finally, evidence for immune complexes in pleural effusions and sera was looked for by determination of Clq binding activity. Levels were higher in culture-positive effusions when compared to culture-negative fluids (P = 0.005).K50 opsonic titers showed a positive correlation with CH50 values (P < 0.001) for all fluids tested. Similarly Clq binding activity correlated with C3d levels in effusions of infectious origin (P = 0.05). Recovery experiments using the various bacterial species isolated from culture-positive pleural effusions showed evidence of complement inactivation upon incubation with pooled sera at concentrations of 10(7)-10(8) microorganisms/ml. These results indicate that one important reason for bacterial persistence in empyema may be decreased opsonization secondary to local consumption of complement.

Adult↗

PubMed1977

[Evaluation of the role of circulating antigen-antibody complexes in the pathogenesis of glomerular nephropathies].

Immunofluorescence studies of the glomeruli in patients suffering from glomerulonephritis (GN) suggest the deposit of immune complexes from the circulating blood. Immune complexes were quantitated using a sensitive radioimmunoassay from sera of 41 patients with GN drawn at the time when renal biopsy was performed. Simultaneously, degradation products of C3 (C3d) were measured. Eleven of 12 patients with GN secondary to a systemic disease (usually LED) presented increased C1q-binding activity of their sera (C1q-BA). C3 was further demonstrated in 9 of these patients, suggesting the presence of circulating immune complexes. By contrast only 2 of 12 patients with idiopathic GN characterized by deposits of complement and IgG in the glomeruli exhibited increased C1q-BA. One of 17 patients with idiopathic GN without deposit of immunoglobulins and C3 in the glomeruli also had increased C1q-BA. The results observed in the group of patients with idiopathic GN with glomerular deposits could be accounted for either by a transitory or minimal presence of immune complexes or by local formation of complexes in the glomerular structures.

Antigen-Antibody Complex↗

PubMed1975

[Pathophysiological implications of antigen-antibody complexes (author's transl)].

Seventy years after the description of the Arthus phenomenon, the concept of immune complex mediated pathology is widely recognized in clinical pathophysiology. The availability of methods for the detection of soluble immune complexes opens new paths for clinical investigation in this field. This is demonstrated for systemic lupus erythematosus, viral hepatitis B and herpes zoster disease. New experimental approaches deal with the question of tissue localization of immune complex mediated diseases, e.g. through affinity of antigens for certain tissue structures.

Animals↗