Gliosarcoma--case report and review of the literature.
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Brain Neoplasms↗
Biomedical subjects
R Meyermann
Publications and source records attributed to R Meyermann.
Leukocyte chemotactic factor, a natural ligand to CD4, is expressed by lymphocytes and microglial cells of the MS plaque.
The leukocyte chemotactic factor (LCF) is a proinflammatory cytokine and natural soluble ligand to the human CD4 molecule. LCF is produced by CD4+ and CD8+ T lymphocytes and is considered essential to the influx of CD4+ T lymphocytes and macrophages into an inflammatory lesion. In order to investigate the role of LCF in the multiple sclerosis (MS) lesion, we have used a synthetic gene to express LCF in E. coli and have produced monoclonal antibodies against LCF. Monoclonal antibodies are suited to demonstrate LCF in ELISAs. Western blots and paraffin-embedded tissue sections. In the MS lesion, immunopositive lymphocytes and microglial cells, notably, have been found. This is the first demonstration that LCF is present in MS lesions. Immunostaining of microglial cells is noteworthy, as these cells are strategically placed regulatory elements of CNS immunosurveillance and like other cells of the monocytic lineage express CD4 molecules. Thus, LCF might be a paracrine factor regulating T-lymphocyte chemoattraction and an autocrine molecule regulating microglial cell immune reactivity.
Aged↗
Fatal stroke in a patient with carotid and middle cerebral artery dissection associated with cystic medial necrosis.
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Adult↗
Prolonged corticosteroid-induced remission in primary central nervous system lymphoma: report of a case and review of the literature.
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Adrenal Cortex Hormones↗
Expression of microglial markers in the human CNS after closed head injury.
The loss of neurons after severe closed head injury is not only a consequence of the primary impact but also of secondary damage mechanisms. Among the cell population of the central nervous system microglia is surely a candidate to influence secondary damage mechanisms by releasing cytotoxic cytokines [1]. About microglial reaction in closed traumatic brain injury (TBI), however, no data are available. In contrast to experiments using stab wound injury the covering of the CNS in closed TBI are still intact. We have examined 17 patients who died because of TBI after various times post injury. We studied the expression of antigens which are either permanently present on microglial cells or those which are only facultatively found on activated microglia. Low numbers of microglial cells were shown to express MHC-class II antigens immediately after TBI which is also true for CD 68 and leukocyte common antigen (LCA). Surprisingly, however, antigens such as HAM 56 were expressed not earlier than 72 hours after TBI as well as the lectin ricinus communis agglutinin-1 (RCA-1). The results indicate a delayed activation of microglia in traumatic brain injury.
Adolescent↗
Three siblings with Walker-Warburg Syndrome.
The Walker-Warburg syndrome (WWS) is an autosomal recessive disease entity within the framework of "cerebro-ocular-muscular syndromes". The gene locus is still undetected. Its diagnostic criteria have been firmly established in the literature on newborns or infants affected with the disease. However, a diagnosis of severe pathologic conditions must often be made on the basis of ultrasound examination at a fetal age. It is therefore necessary to examined whether the diagnostic criteria are sufficient to warrant a diagnosis at the fetal stage. We here report on a new family affected with WWS. Two elder siblings had presented with epileptic seizures, eye abnormalities as well as multiple skeletal dysplasias (the latter finding in the first child only) in the neonatal period, and died in their first years. Postmortem examination of the second child revealed type II lissencephaly, buphthalmos, and undifferentiated retina with rigid retinal folds. Skeletal muscle tissue was not examined. In a sibling fetus, bilateral cataract was detected in the 17th gestational week by ultrasonographic examination. Postmortem examination in the 23rd gestational week revealed type II lissencephaly and bilateral cataract. Skeletal muscle was normal. Taken together, all siblings were diagnosed as Walker-Warburg syndrome. In the fetal case, prenatal diagnosis could only be made with confidence against a background of a positive family history.
Abnormalities, Multiple↗
Immunolocalization of vgr (BMP-6, DVR-6), a TGF-beta related cytokine, to Schwann cells of the rat peripheral nervous system: expression patterns are not modulated by autoimmune disease.
The transforming growth factors type beta (TGF-beta) have been implicated in regulation of peripheral nervous system inflammation and regeneration. Here we demonstrate expression of a TGF-beta-related bone morphogenetic protein, the vgr (BMP-6, DVR-6) in Schwann cells of the rat peripheral nervous system. The expression of vgr in the peripheral nervous system suggests that this factor and probably other TGF-beta-related bone morphogenetic proteins might participate in Schwann cell function during aspects of peripheral nervous system physiology and pathology. However, we did not observe changes in expression patterns in response to autoimmune inflammation (experimental autoimmune neuritis) of the peripheral nervous system.
Amino Acid Sequence↗
Neutrophilic defensins penetrate the blood-brain barrier.
Defensins are small, cationic, cyclic peptides that are abundantly stored in granules of neutrophils. Defensins non-specifically interact with membranes by forming weakly ion-selective pores. Here we demonstrate immunolocalization of defensin-secreting cells in human brain. Defensins, secreted by activated granulocytes, apparently are not prevented by the blood-brain barrier (BBB) from diffusing across cerebral endothelium to penetrate the neuropil for a considerable distance from the granulocyte. This is in contrast to other neutrophil proteins like the granule-associated enzyme elastase or the cytosolic protein MRP-14, which are strictly localized to the cytoplasm or granules of neutrophils. Thus, defensins, known chemokinetic and chemotactic molecules, display a unique distribution at BBB sites.
Antibodies, Monoclonal↗
Detection of two transforming growth factor-beta-related morphogens, bone morphogenetic proteins-4 and -5, in RNA of multiple sclerosis and Creutzfeldt-Jakob disease lesions.
The bone morphogenetic proteins (BMPs) constitute a novel subfamily of the transforming growth factor type beta (TGF-beta) supergene family. Here we demonstrate, using polymerase chain reaction (PCR) BMP-4 and BMP-5 messages in RNA isolated from multiple sclerosis (MS) plaque tissue. This is the first demonstration of BMP expression in an inflammatory lesion in general, and in MS in particular. However, BMP-4 and BMP-5 messages could be detected in RNA isolated from a Morbus Creutzfeldt-Jakob (CJD) lesion. Even in normal brain, RNA expression of BMP-4, but not that of BMP-5, was detected. Therefore, BMP-5 gene expression seems to be associated with MS and CJD lesions, whereas the BMP-4 gene appears to be constitutively expressed in the human brain. As TGF-beta s and BMPs are regulators of regenerative processes and contribute to regulation of chemoattraction and local immunoreactivity, BMP-4 and BMP-5 might be involved in aspects of MS lesion formation unknown so far. PCR analysis of human cell lines demonstrate BMP-4 and BMP-5 expression in leukocytic cells, suggesting that infiltrating leukocytes contribute at least in part to BMP-4 and BMP-5 mRNAs of the MS plaque.
Creutzfeldt-Jakob Syndrome↗
Immunocytochemical localization of glycogen phosphorylase in primary sensory ganglia of the peripheral nervous system of the rat.
Neuronal localization was investigated of glycogen phosphorylase (GP) in ganglia of the peripheral nervous system of the rat. Immunofluorescence and immunoenzymatic procedures were applied with a monoclonal anti-bovine brain GP antibody on paraformaldehyde-fixed, paraffin-embedded tissues. Immunoreactivity was only present in the somatic neurons of the mesencephalic trigeminal nucleus in the brain stem and in dorsal root ganglia (DRG), but not in the autonomic neurons of the superior cervical ganglia or in the sensory nuclei of the spinal cord. GP immunoreactivity was present as early as day 1 after birth. In the adult rat, staining was present in neurons of different sizes, and to varying intensities. No relationship was apparent between the staining intensities and morphologically distinguishable types of neurons. In DRG, the type of reactivity was the same from cervical to sacral ganglia. The selected occurrence of GP in specific neurons of the peripheral nervous system in contrast to the ubiquitous occurrence in all astrocytes of the central nervous system may indicate a different role of neuronal glycogen compared to astrocytic glycogen.
Animals↗
Immunolocalization of BMP-6, a novel TGF-beta-related cytokine, in normal and atherosclerotic smooth muscle cells.
We have analyzed expression of a novel transforming growth factor type beta (TGF-beta)-related cytokine, bone morphogenetic protein-6 (BMP-6) in normal and atherosclerotic brain arteries. BMP-6 immunoreactivity was detected in smooth muscle cells of normal cerebral blood vessels. It is also expressed by smooth muscle cells of intimal plaques in atherosclerotically changed blood vessels. The BMPs regulate tissue modeling and remodeling and aberrant expression of BMPs might contribute to smooth muscle cell migration, proliferation, tissue reorganization and macrophage attraction, which are known mechanisms of atherosclerotic plaque formation.
Amino Acid Sequence↗
The antidepressant rolipram suppresses cytokine production and prevents autoimmune encephalomyelitis.
In multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) the cytokines tumour necrosis factor-alpha (TNF), lymphotoxin-alpha (LT), and interferon-gamma (IFN-gamma) are of central pathogenetic importance. A therapy capable of stopping neurological deterioration in MS patients is not yet available. Here, we report that rolipram, a selective type IV phosphodiesterase inhibitor, stereospecifically suppresses the production of TNF/LT and less strongly also IFN-gamma in human and rat auto-reactive T cells. Moreover, we show that rolipram is an effective treatment for EAE. Rolipram has extensively been studied in humans for the treatment of depression, but has not yet been marketed. The data presented here identify rolipram as potential therapy for multiple sclerosis and provoke the immediate initiation of clinical trials.
Animals↗
Reactive microglia in Creutzfeldt-Jakob disease.
Creutzfeldt-Jakob disease (CJD) is characterized by a loss of neurons accompanied by astrogliosis and spongiform changes in the neuropil. It has been recognized that reactive microglia occur in CJD but little is known about the regional distribution and extent of the microglial activation. We have, therefore, examined six brains from cases of sporadic CJD by immunohistochemical labelling of grey and white matter microglia from frontal, parietal, temporal, and occipital lobes, striatum, thalamus, cerebellum and brain stem with RCA-1, LCA, CD68, HLA-DR, and HAM56. Microglial activation occurred in the grey matter where astrogliosis and prion protein (PrP) deposits were prominent. Processes of activated microglia surrounded the outer rim of spongy vacuoles. A diffuse microglial response was seen in the white matter that was immunophenotypically different from grey matter. Double-labelling with microglial markers and anti-PrP showed that activated microglia did not contain PrP-immunoreactivity. Therefore a primary role of microglia in PrP processing seems unlikely. Activated microglia may contribute to neuronal damage in CJD due to their cytotoxic potential.
Aged↗
Expression of BMP-6, a TGF-beta related morphogenetic cytokine, in rat radial glial cells.
Bone morphogenetic protein-6 (BMP-6) is a member of the TGF-beta superfamily of cytokines. The bone morphogenetic proteins and homologous cytokines participate in realization of the genetic body plan by regulating homeotic gene expression, embryonic development, and neurogenesis. Here we demonstrate expression of BMP-6 in rat radial glial cells which are involved in embryonic organisation of the central nervous system. Thus, morphogenetic cytokines like BMP-6 might contribute to radial glial cell function in organizing the migration of immature neurons during the development of the CNS cortex.
Amino Acid Sequence↗
Perforin and tumor necrosis factor alpha in the pathogenesis of experimental allergic encephalomyelitis: comparison of autoantigen induced and transferred disease in Lewis rats.
A cell-mediated cytotoxic reaction is believed to be involved in inflammatory lesion formation of experimental allergic encephalomyelitis (EAE). We compared EAE diseased animals which had either been immunized with myelin basic protein (MBP) or adoptively received MBP specific T-cell lines in order to study whether the different courses of disease induction are reflected by quantitative or qualitative differences in the expression of genes encoding putative mediators of tissue damage, i.e. TNF alpha, and the pore-forming protein perforin. With the appearance of signs of paralysis, both genes are induced in cells within the CNS lesions, whereas drastically reduced numbers of TNF alpha- and perforin gene-expressing cells are observed during recovery, despite the presence of high numbers of mononuclear cells in the CNS. Marked differences, however, exist in the gene expression profiles: during the phase of most severe clinical signs TNF alpha expressing cells are 2 to 3 times more frequent in transferred than immunized animals. In animals with MBP-induced EAE the number of perforin expressing cells represents only 1.6% of the IL2R gene expressing cells, while this fraction represents 25% in mice which received autoaggressive T cells. Thus, the presence of a high number of activated killer cells may accelerate tissue damage and progression of disease in passive EAE whereas in actively induced EAE activation of regulatory mechanisms induced by polyclonal activation after immunization may prevent generation of large amounts of activated cytotoxic T cells.
Animals↗
Glycogen phosphorylase activity and immunoreactivity during pre- and postnatal development of rat brain.
Catalytic activity and immunoreactivity of glycogen phosphorylase were studied in pre- and postnatal rat brain. The catalytic activity was assayed in brain homogenates; immunoreactivity was investigated by immunoblot analysis using a monoclonal anti-bovine brain glycogen phosphorylase antibody. The cellular localization and intensity of immunoreactivity were analysed on paraffin-embedded sections utilizing the same monoclonal antibody. The catalytic activity increased 10-fold from embryonic day 16 to adult; immunoreactivity became detectable on embryonic day 16 and increased in intensity as the enzyme activity rose to adult values. The first cellular elements to be stained immunohistochemically were ependymal cells lining the ventricles, ependymal cells of the choroid plexus, meningeal cells and a selected population of neurons in the brain stem. The immunoreactivity of plexus cells and meningeal cells was reduced or absent in the adult rat brain. The earliest appearance of glycogen phosphorylase immunoreactivity in astroglial cells was seen at postnatal day 9 in the hippocampus. The staining pattern of the adult brain was reached at day 22 post partum. The developmental changes in glycogen deposition and in glycogen phophorylase activity and immunoreactivity may indicate a variable physiological role of glycogen metabolism for different cell types in the pre- and postnatal periods.
Animals↗
Intercrines in brain pathology. Expression of intercrines in a multiple sclerosis and Morbus Creutzfeldt-Jakob lesion.
Expression of cytokine genes regulating vascular permeability and chemoattraction was studies by polymerase chain reaction in RNA from two different types of brain lesions: a multiple sclerosis plaque and in tissue from a patient with Creutzfeldt-Jakob disease. While cytokine genes encoding vascular permeability factor, interleukin (IL)-2, IL-4, or IL-10, generally associated with active inflammatory processes, were not expressed, we observed expression of some intercrine genes in both types of lesions. As these lesions share a common set of structural features such as prominent astrogliosis and glial cells are known producers of intercrines, we suggest that intercrines have a role in the formation of gliotic brain lesions.
Aged↗
[Nucleoli in nerve cells and tumor genesis].
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Cell Nucleolus↗