R L Friede

Georg-August-Universität Göttingen, Göttingen, Lower Saxony, Germany

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Publications (108)571.64 Total impact

  • W Brück · Y Brück · B Maruschak · R L Friede
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    ABSTRACT: Monocytes/macrophages are important effector cells in myelin removal during Wallerian degeneration. Experiments with the mouse mutant C57BL/Ola revealed prolonged axonal survival and reduced phagocytic cell recruitment after nerve transsection. In the present study, we compared the course of Wallerian degeneration in peripheral nerves of C57BL and C57BL/Ola mice in vivo and in vitro. In vivo experiments confirmed earlier investigations describing a delayed degeneration in the C57BL/Ola mutant compared with C57BL mice which were used as control animals without abnormal degeneration. Quite different results were seen in experiments in vitro: degenerating nerve segments of C57BL/Ola mice revealed pronounced axonal breakdown even in the absence of non-resident phagocytic cells. There was no difference in vitro compared with degenerating nerves from C57BL mice. The differences observed between the in vivo and in vitro situations suggest that axonal breakdown plays an important role in the initiation of macrophage recruitment to degenerating peripheral nerves.
    No preview · Article · Feb 1995 · Acta Neuropathologica
  • W Brück · Y Brück · U Diederich · R L Friede
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    ABSTRACT: The present investigation introduces an in vitro model to study macrophage properties during demyelination. Rat dorsal root ganglia (DRG) were cultured for obtaining myelinated peripheral nerve fibers. These cultures were exposed to non-resident macrophages. In untreated control cultures, there was no indication of myelin removal by the added macrophages. DRG were exposed to enzymatically generated oxygen radicals using the xanthin/xanthin oxidase or the glucose/glucose oxidase system. Assessment of Schwann cell viability and ultrastructural morphology revealed different patterns of cell cytotoxicity and morphological changes in different experiments. High concentrations caused complete tissue necrosis of the DRG, while low concentrations did not affect either cell viability or ultrastructural morphology. Under intermediate experimental conditions, oxygen radicals caused non-lethal Schwann cell damage leading to Schwann cell retraction and myelin sheath rejection. Myelin lamellae were disrupted and decompacted. These changes were followed by a selective macrophage attack on myelin sheaths, resulting in demyelination. Axons, Schwann cells and sensory ganglion cells survived this attack. The specificity of the oxygen radical effects was tested in experiments using the oxygen radical scavengers catalase and superoxide dismutase. Catalase prevented the described effects on cell morphology and subsequently blocked demyelination by non-resident macrophages.
    No preview · Article · Feb 1994 · Acta Neuropathologica
  • W Brück · Y Brück · Brigitte Maruschak · Reinhard L. Friede
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    ABSTRACT: The present study introduces an in vitro model of xenogeneic peripheral nerve rejection to analyze the role of macrophages in this complex immunological situation. Nerve-sensitized mouse peritoneal exudate cells were co-cultured with rat peripheral nerve segments. The cultured rat nerve segments were fulminantly rejected in vitro by the co-cultured mouse peritoneal cell population. The massive tissue destruction included Schwann cell damage and was quite distinct from basic myelin phagocytosis observed during Wallerian degeneration in earlier experiments. The nerve-sensitized peritoneal exudate consisted of macrophages and T-cells. Antibody depletion experiments were performed to analyze T-lymphocyte effects in this model. Fulminant tissue rejection depended on the presence of T-lymphocytes in the culture medium. Their presence at the immediate site of tissue rejection, however, was not required. Further experiments were aimed at defining the role of T-cell-derived mediators during in vitro rejection. Depletion experiments using a panel of antibodies to cytokines revealed a critical involvement of IL-2, IL-3, IL-4, IL-6 and interferon-gamma in the induction of tissue rejection in vitro. Fulminant tissue rejection in vitro depended on the interaction of these cytokines with macrophages. The participation of macrophage surface receptors was studied in another series of experiments. The macrophage complement receptor type 3 was shown to be critically involved in the phagocytic attack during rejection. Antibodies to MHC class II antigens also abolished fulminant in vitro rejection, indicating that continuous antigen presentation is required in this process.
    No preview · Article · Feb 1994 · Journal of Neuropathology and Experimental Neurology
  • R L Friede · W Brück

    No preview · Article · Feb 1993 · Advances in neurology
  • W Brück · Y Brück · R L Friede
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    ABSTRACT: Mononuclear cells of the monocyte/macrophage system play an important role in myelin ingestion during Wallerian degeneration. The present in vitro study clarifies the role in this process of two macrophage-secreted cytokines, TNF-alpha and interleukin-1. Treatment with TNF-alpha massively reduced the amount of myelin ingested by macrophages via their complement receptor type 3 (CR3). Anti-TNF-alpha antibodies reversed the effect. Immunofluorescence of macrophages indicated that TNF-alpha caused a reduced expression of the CR3 by phagocytic cells. Further experiments revealed an interaction of TNF-alpha with its receptor on the macrophage cell membrane. Interleukin-1 had no effect on myelin ingestion in the in vitro system used in these experiments.
    No preview · Article · Jun 1992 · Journal of Neuroimmunology
  • W BRUCK · Y BRUCK · R.L. Friede
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    ABSTRACT: Mononuclear cells of the monocyte/macrophage system play an important role in myelin ingestion during Wallerian degeneration. The present in vitro study clarifies the role in this process of two macrophage-secreted cytokines, TNF-alpha and interleukin-1. Treatment with TNF-alpha massively reduced the amount of myelin ingested by macrophages via their complement receptor type 3 (CR3). Anti-TNF-alpha antibodies reversed the effect. Immunofluorescence of macrophages indicated that TNF-alpha caused a reduced expression of the CR3 by phagocytic cells. Further experiments revealed an interaction of TNF-alpha with its receptor on the macrophage cell membrane. Interleukin-1 had no effect on myelin ingestion in the in vitro system used in these experiments.
    No preview · Article · May 1992 · Journal of Neuroimmunology
  • Ragnhild Rössing · Reinhard L. Friede
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    ABSTRACT: The authors report holoprosencephaly combined with an enormous extracerebral glio-ependymal cyst in the superior cistern of a 10-week-old boy. The cyst had compressed the holosphere at the floor of the anterior fossa and had caused herniation of the cerebellar vermis and tonsils at the foramen magnum, along with ascending cervical roots. This uncommon combination of lesions clinically may mimic hydranencephaly or hydrocephalus. Holoprosencéphalie avec kyste extra-cérébral rétroproencéphalique Les auteurs rapportent le cas d'une holoproencéphalie associée a un énorme kyste glioépendymaire extracérébral de la citerne supérieure, chez un garçon de dix semaines. Le kyste avait comprimé les hémisphères sur le plancher de la fosse antérieure et avait causé une hernie du vermis et des amygdales cérébelleux dans le trou occipital, ainsi que des racines cervicales ascendantes. Cette combinaison inhabituelle de lésions peut simuler cliniquement une hydranencéphalie ou une hydrocéphalie. Holoprosenzephalie mit retroprosenzephaler extrazerebraler Zyste Die Autoren berichten über eine Holoprosenzephalie in Verbindung mit einer sehr großen extrazerebralen glioependymalen Zyste in der Cisterna superior bei einem 10 Wochen alten Jungen. Die Zyste hatte das Gehirn am Boden der Fossa anterior komprimiert und eine Herniation des Kleinhirnwurmes und der Kleinhirntonsillen am Foramen magnum entlang der aufsteigenden zervikalen Wurzel verursacht. Diese ungewöhnliche Kombination kann klinisch eine Hydranenzephalie oder einen Hydrozephalus vortäuschen. Holoprosencefalia con quiste extracerebral retroprosencefálico Los autores aportan una holoprosencefalia combinada con un enorme quiste extracerebral glioependimal, a nivel de la cisterna superior en un muchacho de 10 semanas de edad. El quiste habia comprimido la holosfera a nivel del suelo de la fosa anterior y habia causado herniación del vermis cerebeloso y de las amigdalas a través del foramen magnum, a lo largo de la raiz cervical ascendente. Esta rare combinación de lesiones puede parecer clinicamente una hidranencefalia o un hidrocéfalo.
    No preview · Article · Mar 1992 · Developmental Medicine & Child Neurology
  • Wolfgang Brück · Ulrich Sander · Peter Blanckenberg · Reinhard L. Friede
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    ABSTRACT: Xanthogranulomas involving the choroid plexus of the lateral ventricles are generally asymptomatic lesions. The case is reported of a 50-year-old man in whom a xanthogranuloma of the choroid plexus had occluded the left trigone, causing unilateral hydrocephalus of the left temporal horn and neurological symptoms. A review of the literature shows that xanthogranulomas of the glomus of the lateral ventricles differ from the xanthomatous cystic lesions of the third ventricle, which are probably akin to colloid cysts.
    No preview · Article · Sep 1991 · Journal of Neurosurgery
  • A Reles · R L Friede
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    ABSTRACT: The relationship between the degree of nodal narrowing and the changes in the structure of the axonal cytoskeleton was studied in 53 fibres of mouse sciatic nerve. Nodal narrowing increased with increasing fibre calibre to reach about 20% of the internodal area in the thicker fibres. The narrowing corresponded quantitatively to a decreased number of nodal neurofilaments. Nodal microtubule numbers varied greatly, and a majority of fibres had considerably (approximately 55%) more microtubules in their nodal profile than in the internode. Nodal profiles of different calibre showed an increase in the number of filaments and of microtubules with nodal calibre, although at rates different from those in the internode. The degree of observed axon non-circularities had no discernible effect on the restructuring of the axonal cytoskeleton at the node. A transnodal transport of the axonal cytoskeleton can occur with: (1) accelerated transnodal transport of filaments, (2) stationary internodal fraction of filaments, (3) depolymerization of filaments proximal to the node and repolymerization distally, or (4) different nodal and internodal polymerization equilibria.
    No preview · Article · Jul 1991 · Journal of Neurocytology
  • W Brück · R.L. Friede
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    ABSTRACT: Myelin removal in nerves undergoing wallerian degeneration mainly depends on invading, non-resident macrophages. The present study clarifies the role of serum complement components in this process in vitro and in vivo. Macrophages cocultured with degenerating nerves in vitro were unable to invade these nerves in the presence of C3-deficient serum. Application of C3-deficient serum subsequent to cellular invasion abolished the myelin phagocytic capacity of the invaded macrophages. This indicates that opsonization of myelin by complement components is necessary in myelin ingestion via macrophage receptors. In vivo, a monoclonal antibody to the macrophage complement receptor type 3 (CR3) significantly reduced myelin phagocytosis. Immunohistochemistry with anti-C3 antibodies showed a marked reaction in degenerating nerves. Immunoelectron microscopy localized C3 particles at the degenerating myelin sheaths. Haematogenous cells, invading the degenerating nerves, also showed a strong reaction for C3 in their cytoplasm. These results indicate that complement components play a critical role both in macrophage invasion of degenerating nerves and in the ingestion of myelin by these cells.
    No preview · Article · Jul 1991 · Journal of the Neurological Sciences
  • K Karyofilis · R L Friede
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    ABSTRACT: The incidence of oxytalan fibres was studied in 202 meningiomas and 30 neomembranes. Oxytalan fibres were present in all samples of neomembranes and in the majority of meningiomas; 81% of the fibroblastic meningiomas contained oxytalan fibres. Their frequency was lowest in malignant meningiomas.
    No preview · Article · Feb 1991 · Acta Neuropathologica
  • W Brück · H J Christen · H Lakomek · F Hanefeld · R L Friede
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    ABSTRACT: We report on a 3 3/4-year-old girl with acute lymphoblastic leukemia. Polychemotherapy caused a complete remission of the tumor. Six months after treatment was started, the patient developed vomiting and diarrhea necessitating parenteral nutrition. Disturbance of eye movements appeared 4 weeks later. The patient died suddenly 3 days after their manifestation. Autopsy revealed Wernicke's encephalopathy. This case demonstrates the need for thiamine substitution in infants with malignant diseases.
    No preview · Article · Jan 1991 · Clinical neuropathology
  • W Brück · R L Friede
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    ABSTRACT: Myelin phagocytosis in nerves undergoing Wallerian degeneration has been shown to depend on their invasion by non-resident, hematogenous macrophages. This process can be studied in vitro using organ cultures of peripheral nerves exposed to cultured peritoneal macrophages. The present report concerns the role of cell surface carbohydrates in the invasion of degenerating nerves and in the recognition and ingestion of myelin by the phagocytic cells. Additional experiments explored the effect of pH, calcium and cytochalasin D on myelin phagocytosis. Organ cultures with peritoneal macrophages were treated with 14 simple or complex sugars or with eight sugar-splitting enzymes. Macrophage invasion was diminished by many simple or complex sugars, but exposure to sugars had no effect on the recognition or ingestion of myelin by the invading macrophages. Macrophage invasion was abolished upon treatment with beta-mannosidase. Exposure to L-fucosidase abolished the myelin phagocytic capacity of invading macrophages completely without affecting their capacity to ingest carbon or latex particles. The results indicate that the phagocytosis of myelin by macrophages is an L-fucosidase-sensitive process, probably by interaction with their complement receptor type C3.
    No preview · Article · Jun 1990 · Journal of Neuroimmunology
  • S Ropte · P Scheidt · R L Friede
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    ABSTRACT: Biophysical studies have shown that the narrow slit between the turns of the myelin leaflet includes a water space lined by strongly negative, fixed charges on the faces of the myelin leaflet. The accessibility of this slit to a marker should depend largely on the interaction between the marker charges and the surface charges on the myelin leaflet. This premise was explored in vitro by comparing the redistribution of anionic ferritin with highly cationized ferritin under a variety of experimental conditions. Cationized ferritin stained the basal lamina and penetrated it. It also bound to Schwann cell membranes, and it entered mesaxons and lodged between myelin lamellae. There was evidence of facilitated particle redistribution due to attractive forces between the cationized ferritin particles and the membrane surfaces. Anionic ferritin did not enter sheaths under identical experimental conditions. Additional experiments reconfirmed X-ray spectrographic data on a loosening of lamellar coherence upon elution of Ca2+ and recompaction of myelin by small amounts of Ca2+. If cationic ferritin was substituted for Ca2+ in these experiments, it also caused recompaction of myelin which had been loosened by previous Ca2+ elution. The cationic ferritin particles sandwiched between the recompacted myelin lamellae. These observations show that the slit between the turns of the myelin leaflet is preferentially accessible to cations, that cations can redistribute along it and that their presence is important for maintaining myelin periodicity. They also throw light on the significance of wide-spaced myelin in pathological conditions.
    No preview · Article · May 1990 · Journal of Neurocytology
  • W Brück · R L Friede
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    ABSTRACT: Myelin phagocytosis in Wallerian degeneration of peripheral nerves depends on invasion of nerves by non-resident macrophages. The present study was done to clarify the role of the macrophage complement receptor type 3 (CR3) in myelin removal. Myelin phagocytic capacity of invading macrophages was abolished by treatment of cultured nerves and macrophages with anti-CR3 antibody or by serum complement depletion with cobra venom factor. This indicates that myelin phagocytosis is mediated by the macrophage CR3.
    No preview · Article · Feb 1990 · Acta Neuropathologica
  • W Brück · R L Friede
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    ABSTRACT: Myelin phagocytosis in nerves undergoing Wallerian degeneration was shown to depend on their invasion by non-resident, hematogenous macrophages. This process can be studied in vitro using organ cultures of peripheral nerves exposed to cultured peritoneal macrophages. The present report concerns the effect of recombinant interferon-gamma (rIFN-gamma) on luminol-dependent chemiluminescence, macrophage migration and myelin phagocytosis in organ cultures. Chemiluminescence was activated by rIFN-gamma compared to untreated cells. The macrophage population was capable of activation at any phase of exposure to organ cultures. The engagement of macrophages in myelin phagocytosis, however, varied with the timing of the application of rIFN-gamma. Application from the start of the experiment led to activation of chemiluminescence and also to a complete inhibition of macrophage invasion of the organ culture, thus preventing myelin removal. Application of rIFN-gamma at a later phase of the experiment had no effect on cell invasion and also no detectable effect on the efficiency of myelin phagocytosis. There was no indication that myelin phagocytosis by itself activated chemiluminescence in untreated cultures. Phagocytosis of myelin appears to be a function of macrophages independent of activation causing production of oxygen radicals.
    No preview · Article · Dec 1989 · Journal of Neuroimmunology
  • E. Bunker · R. L. Friede
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    ABSTRACT: A computer program simulates the changes in a nerve's histogram during normal growth and from various neuropathies. The program shows how a nerve's histogram will change from various percentages of fiber damage or from preferential damage to either thick or thin fibers, or from various degrees of fiber restitution, or from single-event or repetitive damage. In single-event damage, the main alteration is a preponderance of thin (regenerating) fibers. Patterns of selective fiber vulnerability are difficult to deduce from the shape of the histogram. Repetitive damage remodels the histogram to a broad unimodal fiber distribution at reduced mean caliber. Comparison of simulated changes with data from an experimental isoniazid neuropathy yielded a close match between observed changes and simulation.
    No preview · Article · Sep 1989 · Acta Neuropathologica
  • Petra G. Hann Bonnekoh · P Scheidt · Reinhard L. Friede
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    ABSTRACT: Organ cultures of degenerating nerve fascicles were exposed to cultured macrophages obtained by peritoneal lavage. Invasion of the nerve fascicle by phagocytes was shown by prelabeling with carbon and with electron microscopy. There was massive active phagocytosis of degenerating myelin sheaths. The invading phagocytic cell population was identified as Fc receptor-positive, Mac-1-positive macrophages by immunocytochemistry. The Schwann cell population persisted without significant myelin phagocytosis. The vitality of the Schwann cell population was shown by subsequent reimplantation of the organ cultures into host animals. The reimplants had retained their ability to remyelinate regenerating axon sprouts. These observations were made in cultures exposed to cytostatic agents. If cytostatic agents were omitted, there was proliferation of endogenous phagocytes in the nerve fascicles without added peritoneal cells. These endogenous phagocytes were identified as proliferating resident monocytes and were positive for the Fc receptor and Mac-1 markers. This model allows studies on how monocytes recognize and digest degenerating myelin apart from surviving Schwann cells.
    No preview · Article · Apr 1989 · Journal of Neuropathology and Experimental Neurology
  • E Bunker · R L Friede
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    ABSTRACT: A computer program simulates the changes in a nerve's histogram during normal growth and from various neuropathies. The program shows how a nerve's histogram will change from various percentages of fiber damage or from preferential damage to either thick or thin fibers, or from various degrees of fiber restitution, or from single-event or repetitive damage. In single-event damage, the main alteration is a preponderance of thin (regenerating) fibers. Patterns of selective fiber vulnerability are difficult to deduce from the shape of the histogram. Repetitive damage remodels the histogram to a broad unimodal fiber distribution at reduced mean caliber. Comparison of simulated changes with data from an experimental isoniazid neuropathy yielded a close match between observed changes and simulation.
    No preview · Article · Feb 1989 · Acta Neuropathologica
  • K Tamagawa · P Scheidt · R L Friede
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    ABSTRACT: Subarachnoid heterotopias were produced experimentally in rats by intracisternal injection of dissociated fetal brain tissue. Heterotopias contained neurons and glial tissue and also mesodermal tissue including striated skeletal muscle. The data show that particles of disintegrated germinal tissue can survive, redistribute, settle and mature within the CSF spaces.
    No preview · Article · Feb 1989 · Acta Neuropathologica

Publication Stats

3k Citations
571.64 Total Impact Points

Institutions

  • 1982-1995
    • Georg-August-Universität Göttingen
      • Division of Agroecology
      Göttingen, Lower Saxony, Germany
  • 1982-1988
    • Universitätsmedizin Göttingen
      • Department of Neuropathology
      Göttingen, Lower Saxony, Germany
  • 1985
    • Johannes Gutenberg-Universität Mainz
      • Department of Neuropathology
      Mayence, Rheinland-Pfalz, Germany
  • 1981
    • University Hospital Zürich
      Zürich, Zurich, Switzerland
  • 1977-1981
    • University of Zurich
      • Institute of Veterinary Pathology
      Zürich, Zurich, Switzerland