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Biomedical subjects

H Kolb

Publications and source records attributed to H Kolb.

At least 307 records · Page 17Linked to original sources
PubMed1984

Role of carbohydrates in rat leukemia cell-liver macrophage cell contacts.

The mechanism by which macrophages recognize tumor cells is still unknown. We have studied interactions between rat liver macrophages and rat L 5222 leukemia cells. These tumor cells, but not normal leukocytes or erythrocytes, adhere to freshly isolated macrophages in vitro. Binding of tumor cells by macrophages can be inhibited by N-acetyl-D-galactosamine, D-galactose and more potently by glycoproteins with terminal N-acetyl-D-galactosamine or D-galactose residues. Tumor cell adhesion is calcium-dependent. The relevant leukemia cell membrane structures which bear terminal beta-D-galactosyl or related residues have been determined as trypsin- and pronase-sensitive, and hence may presumably be glycoproteins. The tumor cell receptor on liver macrophages appears to be a lectin with the carbohydrate specificity N-acetyl-D-galactosamine greater than D-galactose greater than L-fucose.

Acetylgalactosamine↗
PubMed1984

Amacrine cells in scotopic vision.

Signals from rod bipolar cells of cat retina are processed by a variety of rod amacrine cells before finally arriving at ganglion cells. Three of these rod amacrine cells (AII, A13, and A17 ) have been studied at the physiological and anatomical levels; the results suggest that each carries out a unique visual function: AII cells appear to quicken the response time of the rod system in the mid-scotopic range, while A17 cells may increase the light-gathering area of rod bipolars near visual threshold. Stimulation of A13 cells may disinhibit ganglion cells, thus heightening their responsiveness at low levels of illumination.

Animals↗
PubMed1984

Cell mediated immunity to islet cells: lessons from animal studies.

As a pathogenic factor of type I (insulin-dependent) diabetes cell mediated immunity to pancreatic islet cells, i.e. lymphocytic insulitis has been studied in mice with spontaneous lupus-like autoimmune disease, in mice with experimentally induced immune dysregulation and in mice treated with multiple low doses of streptozotocin or with alloxan. The following conclusions have been reached: Autoimmunity to B-islet cells requires a disturbed immune system. Autoimmune insulitis requires altered B-islet cells. Cellular immunity to B-islet cells apparently involves two different mechanisms: The intrainsular invasion of single lymphocytes and macrophages and the mostly periinsular/periductular infiltration of large numbers of lymphocytes and macrophages. Some observations indicate a primary role of helper and suppressor T lymphocytes as well as of macrophages in B-islet cell destruction. In this paper an attempt will be made to combine observations on the induction and course of insulitis in several animal models in a general scheme of pathological events. Several conclusions on the mechanism of islet autoimmunity have been reached. At the time being however, these "lessons" must be regarded as hypotheses, which may be helpful in understanding the pathogenesis of human type I diabetes.

Animals↗
PubMed1983

Identification of a receptor for senescent erythrocytes on liver macrophages.

Isolated rat liver macrophages adherent to culture dishes phagocytize selectively senescent rat erythrocytes as well as in vitro aged rat erythrocytes but not young or freshly isolated erythrocytes. Since in vitro aged erythrocytes lack cell bound antibodies and phagocytosis occurs in serum free medium, antibodies do not appear to play a role. Phagocytosis as well as binding of old erythrocytes to liver macrophages is inhibited by N-acetyl-D-galactosamine and related monosaccharides (1-25 mM range) and by corresponding synthetic glycoproteins (10(-6)-10(-10) M range) but not by D-mannose or N-acetyl-D-glucosamine. We conclude that recognition and phagocytosis of senescent and in vitro aged erythrocytes is mediated by the galactose particle receptor on rat liver macrophages.

Acetylgalactosamine↗
PubMed1983

Galactose-particle receptor on liver macrophages. Quantitation of particle uptake.

Liver macrophages have been shown previously to bind and ingest gold particles coated with asialoglycoproteins via a N-acetyl-D-galactosamine / D-galactose-specific lectin (Kolb-Bachofen, V., Schlepper-Schäfer, J., Vogell, W. and Kolb, H. (1982) Cell 29, 859-866). We present here a quantitative analysis of lectin-dependent particle endocytosis. We used a conjugate of asialofetuin with colloidal gold as ligand, the cellular uptake of which could be followed by spectrophotometry. Freshly isolated Kupffer cells from the rat liver ingest asialofetuin at a rate of approx. 4200 particles/cell per min. Uptake is inhibited by saccharides related in structure to D-galactose and depends on the presence of Ca2+. The rate of endocytosis is zero below 10 degrees C, shows a modest increase until 20 degrees C and a steep increase between 20 and 37 degrees C. Uptake is energy-dependent and strongly inhibited by cytochalasin B but only slightly by colchicine.

Animals↗
PubMed1983

Two galactose-specific receptors in the liver with different function.

In the rat liver both hepatocytes and macrophages have been shown to express on the surface lectins with similar binding specificity for galactose residues. Functionally the two lectins differ in the uptake of ligands. Whereas the hepatocytes ingest molecules and small particles (less than 10 nm), the macrophages take up particles only. Antisera raised against hepatic galactose-specific receptor failed to react with the macrophage lectin but blocked ligand binding to the hepatocyte only, indicating either a different antigenic structure or membrane localization of the two lectins.

Animals↗
PubMed1983

An epithelial cell line with elongated myoid morphology derived from bovine mammary gland. Expression of cytokeratins and desmosomal plaque proteins in unusual arrays.

Cells of a clonal line (BMGE + HM) selected from bovine mammary gland epithelial cell cultures are described which, after reaching confluence, do not assume typical epithelioid morphology, but form elongated cells with long slender processes extending over the surfaces of other cells. However, cells of this line which display non-epithelioid morphology and are exceptionally rich in actin microfilaments are identified as epithelial cells by their synthesis of cytokeratins and desmosomal plaque proteins, as demonstrated by immunofluorescence and immunoelectron microscopy and by gel electrophoresis of cytoskeletal proteins. The cells do not produce vimentin and desmin filaments. The specific cytokeratin polypeptides of these myoid cells are identical to those present in normal epithelioid BMGE + H cells but are arranged in unusual arrays of meshworks of finely dispersed, non-fasciated filaments and granular structures. Desmosomal plaque proteins, notably desmoplakins, are abundant, but the electron microscopic appearance of the desmosomes is abnormal in that most of them are associated with a second accessory plaque formed at a distance of 0.1-0.15 micron from the normal desmosomal plaque. Both cytokeratin filaments and desmosomal structures are found throughout the whole cytoplasm, including the extended cell processes. The existence of an epithelial cell line with such an unusual morphology demonstrates the importance of non-morphological criteria in identifying epithelium-derived cells. Our findings also indicate that dramatic differences of cell shape and organization of epithelial cells need not necessarily be associated with changes in the expression of specific cytoskeletal proteins. The possible origin of this cell line from myoepithelial cells is discussed.

Animals↗
PubMed1983

Receptor-mediated particle uptake by liver macrophages. The galactose-particle receptor mediates uptake via coated and also non-coated structures.

The endocytosis pathways of particles with terminal beta-D-galactosyl groups were studied in isolated rat Kupffer cells by electron microscopy. Colloidal gold particles of sizes 5, 17 and 50 nm were coated with asialofetuin (ASF) and isolated liver macrophages were allowed to bind (at 4 degrees C) or take up (at 37 degrees C) these ligands. Particles of all three sizes were bound via the galactose-particle receptor as shown by carbohydrate inhibition experiments and were ingested effectively. But, whereas ASF-gold particles of sizes 5 and 17 nm are taken up via the coated pit/coated vesicle pathway, the 50 nm particles are not. These enter the cell via non-coated endocytic vacuoles. All three particle sizes are transported to the same lysosomal compartment. These observations demonstrate that at least in macrophages one receptor is capable to mediate endocytosis via two different pathways depending on ligand size and/or valency.

Animals↗
PubMed1983

Synaptic patterns and response properties of bipolar and ganglion cells in the cat retina.

After intracellular recording, bipolar cells of the cat retina have been stained with HRP and their contacts in the outer and inner plexiform layers examined by electron microscopy. Rod bipolars and cone bipolar cb6 make invaginating, ribbon related contacts with photoreceptors, hyperpolarize in response to light, and have axons terminating in layer b of the IPL. The axon terminal of cb2 ends in layer a of the IPL and its basal contacts with cones mediate hyperpolarizing light-responses. Cone bipolar cb5 is a center-depolarizing type with an axon ending in layer b but its cone contacts are at semi-invaginating basal junctions. Except for the amacrine-contacting rod bipolar cell, all cone bipolar types synapse with both amacrine and ganglion cells in the inner plexiform layer. In addition cb5 contacts AII amacrine cells with large gap junctions, and is physiologically rod dominated.

Animals↗
PubMed1983

Rod pathways in the retina of the cat.

Neurons involved in the transfer of rod signals to the ganglion cells in the retina of the cat have been recorded from and stained with horseradish peroxidase (HRP) and their synaptic connections determined by electron microscopy. The single morphological type of rod bipolar cell responds with a sustained hyperpolarization to light and in turn drives at least five morphologically different types of amacrine cells, each of which has a unique response pattern. Two amacrines respond with either a transient (AII) or a sustained (A17) depolarization to light, while three amacrines give transient (A8) or sustained (A6, A13) hyperpolarizations. Circuitry whereby rod signals reach both on-centre and off-centre ganglion cells is discussed.

Animals↗
PubMed1983

What's new in diabetes? Etiological and pathogenetic aspects of juvenile-onset (type I) diabetes.

In recent years research on the pathogenesis of juvenile-onset, insulin-dependent diabetes mellitus (now called type I) has considerably expanded, a development that is documented by an impressive number of conferences and symposia held on this topic every year. In the present review the authors will discuss new insights into the etiology of type I diabetes. Additional information is available in several recently published reviews.

Adolescent↗
PubMed1983

Suppressive effect of antibodies to immune response gene products on the development of low-dose streptozotocin-induced diabetes.

Low-dose streptozotocin-induced diabetes in mice serves as a model of type I diabetes. Suppression of the development of diabetes (hyperglycemia) in C3H/He mice was achieved with in vivo administration of antibody reactive to Ir-gene products before streptozotocin treatment. A persistent effect was reached with two monoclonal antibodies directed against I-Ak gene products and, surprisingly, by an allo-antiserum to I-J determinants. These results suggest a role for I-A and I-J positive T-lymphocytes and/or macrophages in B-islet cell autoimmunity.

Animals↗
PubMed1983

Insulitis as a consequence of immune dysregulation: further evidence.

Lymphocytic infiltrations in pancreatic islets (insulitis) have been shown previously to occur in mice with spontaneous or experimentally induced immune disorders. We now have studied which type of immune dysregulation leads to insulitis. Immune disorders were induced by treatment with cyclophosphamide (Cy) or phenytoin and by graft versus host reactions (GVHR) across minor or major histocompatibility barriers. Histological analysis of immune disturbed animals revealed insulitis after phenytoin treatment and as a consequence of GVHR. Insulitis during GVHR is only observed in certain mouse strain combinations. Treatment with Cy in a large dose range does not lead to lymphocytic infiltration of pancreatic islets. It is concluded that cellular immunity to islet cells can occur spontaneously during certain types of immune dysregulation. Since phenytoin treatment and GVHR stimulate lymphocytes reactive with major histocompatibility antigens, such structures may also be part of target antigens on islet cells.

Animals↗
PubMed1983

Genetic control of low-dose streptozotocin-induced autoimmune diabetes in mice.

Multiple treatment with low doses of streptozotocin induces in mice an experimental autoimmune diabetes characterized by hyperglycemia and lymphocytic infiltrations of pancreatic islets. We have studied the genetic control of the disease. Low-dose streptozotocin treatment was performed in mice of H-2 congenic strains on B10, C3H, or A background. Blood glucose concentrations were followed up to 100 days. Among the various B10 and C3H strains, significant differences in the development of diabetes (hyperglycemia) are noted demonstrating that genes within the H-2 complex influence the susceptibility to the diabetogenic effect of low-dose streptozotocin treatment. The congenic mouse strains on A background did not differ significantly in the diabetic response to streptozotocin. The analysis of B10 recombinant strains shows that genes coding for susceptibility are located in the centromeric (left) side of the H-2 complex. Evidence for an additional role of non-H-2 genes is given by comparison of mouse strains carrying the same H-2 haplotype on different genetic background genomes: B10.S (H-2s), B10.S(7R) (H-2t2), and C3H.SW (H-2b) are resistant to the diabetic effect of low-dose streptozotocin treatment, whereas A.SW (H-2s), A.TH (H-2t2) and B10 (H-2b) are susceptible to diabetes development.

Animals↗
PubMed1982

The morphology of the bipolar cells, amacrine cells and ganglion cells in the retina of the turtle Pseudemys scripta elegans.

The morphology of the neurons that contribute to the inner plexiform layer of the retina of the turtle Pseudemys scripta elegans has been studied by light microscopy of whole-mount material stained by the method of Golgi. Cells have been distinguished on the basis of criteria that include dendritic branching patterns, dendritic morphology, dendritic tree sizes and stratification of processes in the inner plexiform layer. Many of the neurons have dendritic trees oriented parallel to and a few exhibit an orthogonal orientation with the linear visual streak present in the retina of this species. The neurons of the turtle retina have been compared, where possible, with the neurons of the lizard retina as described by Cajal. The findings are discussed in relation to other vertebrate retinas, and correlations are made with recent electrophysiological recordings of the turtle retina. Comments are made with regard to the significance of orientation of neurons relative to the linear visual streak.

Action Potentials↗
PubMed1982

Light and electron microscopy of the photoreceptors in the retina of the red-eared slider, Pseudemys scripta elegans.

The six different types of photoreceptor in the retina of the turtle Pseudemys scripta elegans have been studied by light and electron microscopy. Fresh whole-mount retina, in which the oil droplet colors of the photoreceptors could be seen, was compared with fixed tissue cut in the vertical plane. The red single cone (large red oil droplet) is largest in diameter and, in electron microscopy (EM) views, has the least opaque oil droplet. It also has a vacuolated paraboloid and a cone pedicle that ends at the intermediate level of the outer plexiform layer (OPL). The green single cone (yellow medium-size oil droplet) has a thinner inner segment and uniformly vacuolated paraboloid. Its cone pedicle ends at the same level as that of red cones. The blue cone (small colorless oil droplet) has an obliquely running axon joining cell body to cone pedicle that lies innermost in the OPL. Double cones are recognizable by their adherent cell bodies and inner segments. The accessory member (green cone) lacks an oil droplet but has a distinct large paraboloid while the principal member (red cone) has an oil droplet (orange) lying more distal than oil droplets of other cone types. The axons of the double cones are separated by glia but have closely apposed pedicles ending above those of the single cones in the outermost level of the OPL. Rod photoreceptors have a large outer segment, no oil droplet, and a low-lying cell body continuous with the pedicle, which ends, like those of the double cones, at the outermost level of the OPL.

Animals↗