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Biomedical subjects

V Kolb-Bachofen

Publications and source records attributed to V Kolb-Bachofen.

119 records · Page 7Linked to original sources
PubMed1981

Hepatic receptor for asialo-glycoproteins. Ultrastructural demonstration of ligand-induced microaggregation of receptors.

Endocytosis of asialo-glycoproteins in hepatocytes is mediated by a lectin-like receptor with specificity for D-galactose. Early events of receptor-ligand interactions have been studied by ultrastructural analysis. Hepatocytes were isolated from the rat liver by collagenase perfusion and incubated with a galactosylated electron dense marker (gold-Gal-BSA, glactosylated bovine serum albumin adsorbed onto colloidal gold particles). Initial binding of gold-Gal-BSA particles occurs to receptors diffusely distributed at hepatic microvilli of the former space of Disé. No lectin activity was found in membrane areas that had formed in situ the region of hepatic cell contact or bile canaliculi. Microaggregation of receptor-ligand complexes is seen as an early consequence of particle binding. Microaggregates contain 2-5 particles and are located outside coated pits. After prolonged incubation larger clusters are formed, these are found associated with coated membrane areas. It is concluded that at least three steps precede the uptake of galactosylated proteins by hepatocytes. These are: (i) binding of ligand at diffusely distributed binding sites; (ii) local microaggregation of receptor-ligand complexes; (iii) formation of larger clusters and association with coated pits.

Animals↗
PubMed1981

Cellular immune reactions against pancreatic islets as a consequence of graft versus host disease.

We studied autoimmune reactions against pancreatic islets occurring as a consequence of defects of the immune system rather than after pathological changes in the endocrine organ itself. Immune dysregulation was induced by transfer of parental lymphocytes into semi-allogeneic F1 recipient mice (graft versus host reaction, GVHR). Recipients were killed 1 month after the induction of the disease. Pancreatic islets were screened by light microscopy for signs of lymphocytic infiltration (insulitis). Severe insulitis was found in all mice undergoing GVHR. The cytotoxic activity of lymphocytes was apparent in electron microscopic studies and affected only B cells. Infiltrations were not seen in the exocrine part of the pancreas nor in heart, liver or kidneys at this early stage of GVHR. It is concluded that non-specific disorders of the immune system induced by GVHR may lead to specific cellular autoimmune reactions against B cells of pancreatic islets.

Animals↗
PubMed1980

Analysis of lectin-dependent recognition of desialylated erythrocytes by Kupffer cells.

Kupffer cells isolated from the rat liver are able to bind neuraminidase-treated rat erythrocytes via a D-galactose-specific receptor on the cell surface. Binding of desialylated erythrocytes was inhibited by several mono- and oligo-saccharides related to D-galactose, but not by unrelated sugars. However, after phosphorylation at position 6 D-glucose was as good an inhibitor as D-galactose. Two synthetic glycoproteins, D-galactosyl-albumin and, at a higher concentration, D-glucosyl-albumin, strongly inhibit cell contacts. Lectin-mediated binding of desialylated erythrocytes is dependent on the presence of Ca2'ons, but independent of ATP formation and cell motility. It is concluded that binding of desialylated erythrocytes by rat Kupffer cells is mediated by a Ca2-dependent D-galactosyl/D-glucosyl-recognition system.

Animals↗
PubMed1980

Spontaneous autoimmune reactions against pancreatic islets in mouse strains with generalized autoimmune disease.

The spontaneously autoimmune mouse strains NZB, NZB X NZW, MRL and BXSB have been examined for signs of autoimmune reactions against islet cells. Between 15 and 55 animals of each strain were tested. Infiltrates of lymphocytes and fibroblasts into pancreatic islets were found in more than 80% of NZB mice, in about 50% of MRL and NZB X NZW mice, and in less than 20% of BXSB mice. Infiltrates were not found in the exocrine portion of pancrea. All NZB mice had abnormal glucose tolerance. In the three other strains between 20 and 50% of animals had abnormal glucose tolerance. All mice had fasting normoglycaemia. The lesions in NZB mice were studied in more detail. It was found by ultrastructural analysis that in young mice pancreatic infiltrates consisted of lymphocytes and fibroblasts. Single lymphocytes were also seen outside the main infiltration area. After 2 to 5 months of age another type of infiltrate, consisting of lymphocytes and macrophages was observed. B-cell destruction by lymphocytes was apparent in both young and adult NZB mice. It is concluded that cellular autoimmune reactions against pancreatic islets may occur spontaneously as a consequence of immunological disorders in NZB, NZB X NZW and MRL mice.

Animals↗
PubMed1979

Autoimmune reactions against liver cells by syngeneic neuraminidase-treated lymphocytes.

We have found that the entrapment of neuraminidase-treated lymphocytes in the liver leads to the induction of autoimmune cellular cytotoxic reactions. Lymphocytes from mouse spleen and thymus were incubated with neuraminidase in vitro and injected i.v. into syngeneic recipients. Lymphocytic infiltrations into the liver were seen 7 days later with both types of cells. After repeated weekly injections of asialo-lymphocytes, destruction of liver tissue became apparent. Electron-microscopic studies showed that hepatocytes, fat storage cells, and endothelial cells were affected, mainly at the hepatic periphery. It is concluded that the adhesion of asialo-lymphocytes to liver cells induces their cytotoxic activity. Similar reactions may occur after paramyxovirus infection due to the action of viral neuraminidase.

Animals↗
PubMed1978

Cellular recognition by rat liver cells of neuraminidase-treated erythrocytes. Demonstration and analysis of cell contacts.

Freshly isolated rat liver cells adhere firmly to neuraminidase-treated rat or mouse erythrocytes but not to untreated erythrocytes. Binding between cells occurs only in the presence of calcium and is specially inhibited by D-galactose. We therefore suggest that cell adherence is mediated by a galactose-specific hepatic membrane receptor. Ultrastructural analysis of contact regions revealed point-like interactions between hepatic microvilli and erythrocytes and no broad areas of membrane contact. When liver cells are cultivated in vitro they lose their ability to bind erythrocytes within 24 h.

Animals↗