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Biomedical subjects

B Bellon

Publications and source records attributed to B Bellon.

At least 73 records · Page 4Linked to original sources
PubMed1983

Albumin, fibrinogen, prothrombin and antithrombin III variations in blood, urines and liver in rat nephrotic syndrome (Heymann nephritis).

Albumin, fibrinogen, prothrombin and antithrombin III (AT III) variations have been studied in blood, urines and liver during an experimental nephrotic syndrome in rats (Heymann nephritis). A quantitative morphometric study (light microscopy) has been performed in the liver using an immunocytochemical technique--(PAP) method--to evaluate the protein synthesis by the number of protein-containing hepatocytes. Some sections were also studied by electron microscopy. The nephrotic animals were compared with control rats. In the blood of nephrotic rats, fibrinogen and prothrombin concentrations were increased and albumin and AT III concentrations were decreased. In the urines of nephrotic rats, albumin, prothrombin and AT III were lost, but no fibrinogen. The morphometric study in the liver has shown a significantly higher number of fibrinogen and prothrombin-containing hepatocytes in nephrotic rats than in controls, suggesting an increased synthesis of these proteins; no change was observed concerning albumin and AT III between nephrotic and control animals. In electron microscopy, albumin was demonstrated in Golgi apparatus, proving that the peroxidase-positive cells are related to protein synthesis. These results show that the mechanisms of regulation of the protein synthesis during nephrotic syndrome are different from one protein to another and, particularly, that their blood level is not the only regulating factor for their synthesis.

Albumins↗
PubMed1983

Relationship between microtubules and Golgi apparatus in hepatocytes: a quantitative study during experimental nephrosis.

In many cell types, microtubules are preferentially associated with the Golgi apparatus. However, the existence of a functional link between these two organelles is still hypothetical. To gain insight into this question, the relationships between microtubules and the Golgi apparatus were studied in rat hepatocytes during experimental nephrosis induced by the aminonucleoside of puromycin. This condition is known to cause prolonged stimulation of plasma protein production by the hepatocytes. Rats were studied 2, 4, 5, 10 and 20 days after aminonucleoside injection. The amount of albumin was measured in serum and hepatic microsomes by laser immunonephelometry. The volume densities of microtubules around the Golgi apparatus and in the remaining cytoplasm were measured by ultrastructural morphometry. Changes of the Golgi apparatus were analysed by measuring the volume density of the whole organelle and the respective proportion of saccules and vesicles. Proteinuria began 5 days after aminonucleoside injection and was accompanied by a decrease in serum albumin and a rise in microsomal albumin. These changes were still more striking after 10 days, but protein and albumin levels were almost back to normal after 20 days. Concomitantly, the volume density of the microtubules increased significantly around the Golgi apparatus (32% after 10 days), and not in the remaining cytoplasm. The Golgi apparatus was enlarged (80% after 10 days) with a higher ratio of secretory vesicle to saccule volume densities. These results show that additional microtubules are present around the Golgi apparatus during the enhanced production of plasma proteins which occurs in nephrosis. They suggest that in hepatocytes, microtubules play a part in the Golgi apparatus function of plasma protein processing.

Animals↗
PubMed1982

Mercuric chloride induced autoimmune disease in Brown-Norway rats: sequential search for anti-basement membrane antibodies and circulating immune complexes.

Mercuric chloride induces in the Brown-Norway rat a biphasic autoimmune disease characterized initially by linear IgG deposits along the glomerular basement membrane followed later by granular IgG deposition. In the present study, anti-glomerular basement membrane antibodies and immune complex-like material were sequentially assessed in serial serum samples. Both were transiently found at the same period. Glomerular linear IgG deposits were present on day 11 but circulating anti-glomerular basement membrane antibodies were only found later on day 16. Circulating immune complexes were first detectable on day 8 before the earliest granular IgG deposits were first observed in the spleen vessels on day 16. The disappearance of circulating anti-glomerular basement membrane antibodies and of circulating immune complexes, although HgCl2 injections were pursued, is in agreement with the self-limited character of mercuric chloride induced autoimmune disease and suggests the induction of immunosuppressive mechanisms.

Animals↗
PubMed1982

Permeability of the blood-air barrier to antiperoxidase antibodies and their fragments in the normal rat lung.

The permeability of the blood-air barrier to antiperoxidase (HRP) IgG antibodies (160,000 daltons), F(ab')2 fragments (100,000 daltons) and Fab fragments (50,000 daltons) was studied in the normal rat. The use of isologous and heterologous immunoglobulin G or IgG fragments injected intravenously allowed a sequential study. It was shown that these proteins transfer from the vascular bed towards to interstitium. Evidence was obtained that these proteins crossed the endothelium through interendothelial spaces or structures suggesting transendothelial channels. The alveolar epithelium was found to be an efficient barrier for heterologous and isologous proteins, raising the question of the origin of serum proteins found in the alveolar surface material. Heterologous anti-HRP IgG antibodies and their Fab fragments were also administered intraalveolarly. The alveolar epithelium was found permeable to Fab fragments but not to IgG molecules, suggesting that some serum proteins present in the alveolar lining fluid can be transepithelially reabsorbed.

Animals↗
PubMed1982

Spontaneous circulating immune complex like material in Brown-Norway rats. Role of environmental factors.

Brown-Norway rats maintained under conventional housing conditions showed a significant increase in the C1q binding activity of serum and to a lesser extent of the Raji cell assay whereas no change was observed, in BN rats maintained under specific pathogen free (SPF) conditions. Glomerular IgG deposits were encountered among rats with circulating immune complexes (CIC). This suggests that microbiological environment is a major factor in the spontaneous appearance of CIC which could be of pathogenic significance.

Animals↗
PubMed1982

Trapping of circulating proteins in immune deposits of Heymann nephritis.

The renal distribution of autologous and heterologous albumin and IgG was studied by electron microscopy using peroxidase-labeled conjugates in rats with Heymann nephritis. In addition, the renal distribution of autologous and heterologous antiperoxidase IgG and their F(ab')2 and Fab fragments was detected using peroxidase alone. All of these proteins crossed the glomerular lamina densa and passed into the urinary space by an extracellular pathway through the epithelial slits and the sites of epithelial detachment. The proteins were trapped in subepithelial immune deposits irrespective of the degree of proteinuria and regardless of the molecular weight, the autologous or heterologous origin, and the electric charges of the protein studied. The trapping was transient and easily reversed. These findings suggest that circulating proteins are able to modify the composition of immune deposits, thereby altering the course of immune complex disease.

Animals↗
PubMed1982

Phagocytosis of heat-aggregated immunoglobulins by mesangial cells: an immunoperoxidase and acid phosphatase study.

It has been demonstrated previously that mesangial cells (MC) phagocytose particulate material and nonimmune proteins, but that cells are able to engulf aggregated immunoglobulins (Igs) has not been proven so far. To investigate this cell function, heat-aggregated antiperoxidase (HRP) Igs were injected intravenously into Lewis rats. Sequential immunoelectron microscopic studies revealed that the injected material accumulates progressively in the extracellular compartment from 10 minutes to 5 hours and disappear afterward. This disappearance was related in part to the incorporation of aggregated anti-HRP Igs within phagosomes and phagolysosomes by MC. Quantitation of the phagocytic process showed that it starts as early as 10 minutes after injection and reaches its peak at 2.5 hours. Endocytosis seems to be associated with the sequestration of injected Igs within large cytoplasmic invaginations and with micropinocytosis. To further support these observations, ultrastructural cytochemistry for acid phosphatase activity was performed. Quantitative studies showed that the number of acid phosphatase-labeled lysosomes in MC was up to 7-fold greater in rats receiving aggregated anti-HRP Igs than in noninjected ones. In conclusion, our combined immunoperoxidase and acid phosphatase studies show that MC possess a vacuolar (lysosomal) apparatus capable of handling heat-aggregated Igs. Whether these cells are also operational in the disposal of soluble immune complexes in spontaneous and experimental conditions remains to be proven. In addition, observations suggesting the drainage of macromolecules from mesangium to the juxtaglomerular apparatus and from mesangium to the urinary space are presented.

Acid Phosphatase↗
PubMed1982

Immune complex-mediated lung injury produced by horseradish peroxidase (HRP) and anti-HRP antibodies in rats.

Horseradish peroxidase (HRP) was administered intratracheally to rats with circulating autologous or heterologous anti-HRP antibodies. Intrapulmonary immune complexes containing HRP, anti-HRP antibodies, but no C3, were detected by immunofluorescence from 1 hour to 48 hours with a maximum of 6 hours after antigenic challenge. The concomitant hemorrhagic alveolitis characterized by fibrin deposits and infiltration by polymorphs and macrophages was also maximal after 6 hours. At the ultrastructural level, HRP was easily detected, and HRP-containing immune deposits were demonstrated along the basement membrane in subepithelial and subendothelial localization and in interstitial spaces. These findings suggest a C3 independent mechanism for lung injury mediated by immune complexes formed in situ.

Animals↗
PubMed1981

Immunoenzymatic study of the protein pathway through the glomerular barrier in rat glomerulonephritides.

Circulating anti-horseradish peroxidase (HRP) IgG antibodies were used in the rat to study the glomerular leakage of proteins in glomerulonephritis (GN) induced by aminonucleoside (AN) and in glomerulonephritis induced by mercuric chloride to produce anti-glomerular basement membrane (GBM) antibodies. In ANGN, autologous albumin and fibrinogen were also detected by immunoperoxidase techniques. In both types of GN, the proteins studied were observed in the glomerular urinary space and proximal tubular cells. No channels were visible in the lamina densa. No accumulation of proteins was seen under the epithelial slits that were not closed. In ANGN, accumulation of proteins was observed in the subepithelial space where the podocytes act as a barrier (closed slits, subepithelial blind pockets, areas covered by broad sheets of cytoplasm), but no accumulation was seen in the lamina rara externa under normal or enlarged slits and areas of large epithelial cytoplasm detachment. Statistical analysis showed that in ANGN, at the time of maximal proteinuria, the number of "micropinocytotic" vesicles in the GBM-embedded part of podocytes was not increased as compared with controls. Such vesicles were not labeled. We conclude that in both types of GN, the permeability of the GBM is diffusely increased and that the plasma proteins pass into the urinary space via an extracellular pathway.

Animals↗
PubMed1980

A search for circulating immune complex-like material during the course of autoimmune complex glomerulonephritis in Lewis and Brown Norway rats.

Circulating immune complexes were repeatedly searched for using the C1q-binding assay and the Raji cell test in Lewis and BN rats immunized with the Fx1A fraction from convoluted proximal tubule or with kidney homogenate, mixed with various adjuvants. An autoimmune glomerulonephritis was easily induced in Lewis rats. A potent adjuvant and a booster injection were necessary to obtain such a glomerulonephritis in the BN strain which is reputedly resistant. No circulating immune complex-like material could be found in Lewis rats using the C1q-binding assay. A high C1q-binding activity was found in Bn rats including control rats. The Raji cell test was weakly positive in Lewis and BN rats including control rats. This study demonstrates that the classical resistance of BN rats can be overcome if a potent adjuvant is used. Our failure to demonstrate circulating immune complexes suggests that in situ formation of immune deposits, as recently demonstrated in passive Heymann's nephritis, may also be operative in autoimmune complex glomerulonephritis. Other factors than the antigen used can be responsible for positive C1q-binding or Raji cell tests.

Animals↗
PubMed1979

Experimental immune glomerulonephritis induced in the rabbit with streptococcal vaccine.

Heavy C3 glomerular deposits were observed in rabbits injected intravenously with C5 streptococcal vaccine. Immunoglobulin deposits appeared later in a few rabbits. Although some data favour the presence of circulating immune complexes during the course of this glomerulonephritis, no evidence for their initiating role could be demonstrated. Streptococcal components are known to activate the alternative pathway of complement. It is suggested that complexes made of streptococcal components and activated C3 might deposit in glomerular tufts.

Agglutinins↗
PubMed1978

Distribution of heterologous antiperoxidase antibodies and their fragments in the superficial renal cortex of normal Wistar-Munich rat: an ultrastructural study.

The distribution of serum proteins in the superficial renal cortex of normal Wistar-Munich rats was studied using a new technique. Heterologous antiperoxidase antibodies (160,000 daltons), their F(ab')2(100,000 daltons), and Fab (50,000 daltons) fragments were injected intravenously and then demonstrated by incubation with free peroxidase after in situ fixation. This technique offered several advantages including easy and uniform detection of the proteins, even in tubular cells, and a high degree of specificity and accuracy. Four findings emerged from this: (1) The glomerular filtration barrier was found to be complete for IgG and incomplete for (ab')2 and Fab fragments. (2) This barrier for IgG was localized in the lamina densa. (3) The filtered proteins were found to be reabsorbed and degraded in the proximal tubule. (4) The three proteins were diffusely detected in the interstitial tissue and in tubular intercellular spaces up to apical tight junctions.

Absorption↗
PubMed1976

Association of overt glomerulonephritis and liver disease: a study of 34 patients.

Thirty-four patients with overt glomerulonephritis and chronic liver disease were studied. Kidney specimens were examined by light, electron and immunofluorescence microscopy. Plasma C3 levels were measured and a search for cryoglobulinemia was carried out in all patients. Twenty-six out of the thirty-four patients had an immune complex type glomerulonephritis (membrano-proliferative glomerulonephritis or glomerulosclerosis with mesangial deposits) suggestive of hepatic glomerulonephritis. The glomerular deposits almost always contained IgA and very frequently other immunoglobulins as well as C3. The membrano-proliferative glomerulonephritis was characterized by severe renal symptoms, mixed cryoglobulinemia and the frequent finding of low C3 levels. These data suggest that there is a linkage between liver disease and glomerulonephritis. The immunomorphological type of glomerulonephritis and the cryoglobulinemia are both suggestive of an immune complex disease. The lowering of the C3 levels could be due to activation of complement components by immune complexes, to hepatic hyposynthesis, or to a combination of the two.

Adult↗
PubMed1975

[The sensitivity of direct and indirect methods in immunofluorescence and immunoperoxidase techniques: a comparative study (author's transl)].

A comparative study of the sensitivities of the immunofluorescence and immunoperoxidase techniques was undertaken. The material used was tissue from experimental and human glomerulonephritis. With the direct method, immunoperoxidase was 10 to 30 times more sensitive than immunofluorescence. However, the sensitivities became equivalent if the level of the labeling in immunofluorescence was equal to or superior to 6. In the indirect method, the sensitivity of the immunoperoxidase technique was one to ten-fold greater than with immunofluorescence.

Animals↗