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  • 1
    Electronic Resource
    Electronic Resource
    Selective accumulation of cyclooxygenase-1-expressing microglial cells/macrophages in lesions of human focal cerebral ischemia (2000)
    Springer
    Acta neuropathologica 99 (2000), S. 609-614 
    Details
    ISSN: 1432-0533
    Keywords: Key words Stroke ; Prostaglandin ; Inflammation ; Tissue remodeling ; Secondary injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cyclooxygenases (COX; prostaglandin endoperoxide H synthases) are key enzymes in the conversion of arachidonic acid into prostanoids which mediate inflammation, immunomodulation, mitogenesis, ovulation, fewer, apoptosis and blood flow. Here, we report COX-1 expression following focal cerebral infarctions (FCI). In healthy control brains, COX-1 was localized by immunohistochemistry to a few endothelial cells, single neurons and rare, evenly distributed brain microglia/macrophages. In infarctioned brains, COX-1+ cells accumulated highly significantly (P 〈 0.0001) in peri-infarctional areas and in the developing necrotic core early after infarction. Here, cell numbers remained persistently elevated up to several months post infarction. Further, clusters of COX-1+ cells were located in perivascular regions related to the Virchow-Robin space. Double-labeling experiments confirmed co-expression of COX-1 by CD68+ microglia/macrophages. Co-expression of the activation antigens HLA-DR, -DP, -DQ (MHC class II) or the macrophage inhibitor factor-related protein MRP-8 (S100A8) by most COX-1+ microglia/macrophages was only seen early after infarction. Thus, COX-1 appeared to be expressed in microglial cells regardless of their activation state. However, the prolonged accumulation of COX-1+ microglia/macrophages restricted to peri-infarctional areas enduring the acute post-ischemic inflammatory response points to a role of COX-1 in tissue remodeling or in the pathophysiology of secondary injury. We have identified localized, accumulated COX-1 expression as a potential pharmacological target following FCI. Therefore we suggest that therapeutic approaches based on selective COX-2 blocking might ¶not be sufficient for suppressing the local synthesis of prostanoids.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051170
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  • 2
    Electronic Resource
    Electronic Resource
    Allograft inflammatory factor-1 defines a distinct subset of infiltrating macrophages/microglial cells in rat and human gliomas (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 673-680 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cell culture ; Cell line ; Glioma ; Calcium-binding proteins ; Microglia enzymology ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Allograft inflammatory factor-1 (AIF-1) is a Ca2+-binding peptide that constitutes a potential modulator of macrophage activation and function during the immune response of the brain. Peptides termed microglia response factor-1 or ionized calcium-binding adaptor molecule-1 have been reported to be identical with AIF-1. We have investigated the expression of AIF-1 in the rat C6 glioblastoma and 9L gliosarcoma tumor models and additionally assessed AIF-1 expression in a diverse range of human astrocytomas by immunohistochemistry. AIF-1 was expressed by activated microglial cells and a subset of infiltrating macrophages in areas of infiltrative tumor growth and in compact tumor areas in both rat and human gliomas. Double-labeling experiments in rats and humans characterized the nature and the functional status of AIF-1+ cells. AIF-1 expression was detected in cells expressing major histocompatibility complex class II molecules and in a subset of activated macrophages/microglial cells. All MRP-8+ cells coexpressed AIF-1. In humans, there was a strong correlation of AIF-1-expressing activated macrophages/microglial cells with tumor malignancy (P 〈 0.0001). These results suggest that AIF-1 defines a distinct subset of tumor-associated activated macrophages/ microglial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010000233
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  • 3
    Electronic Resource
    Electronic Resource
    Intercrines in brain pathology (1993)
    Springer
    Acta neuropathologica 86 (1993), S. 393-396 
    Details
    ISSN: 1432-0533
    Keywords: Multiple sclerosis ; Creutzfeldt-Jakob discase ; Intercrines ; Interleukin-8
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00369453
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  • 4
    Electronic Resource
    Electronic Resource
    Spontaneous multidrug transport in human glioma cells is regulated by transforming growth factors type β (1991)
    Springer
    Acta neuropathologica 81 (1991), S. 641-648 
    Details
    ISSN: 1432-0533
    Keywords: Multidrug resistance ; Glial tumors ; Transforming growth factor type β ; Bone morphogenetic protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The multidrug transporting cell membrane molecule P-glycoprotein can be spontaneously expressed in human glioma cells. Transcripts of mdr genes were detected in glial tumor cells by polymerase chain reaction and Northern blotting, expression of P-glycoprotein was analyzed by immunocytochemistry and functional activity by cytofluorometry of fluorescent probe transport. In vitro treatment of glioma cells with vincristine induced coordinate over-expression of both mdr1 and mdr3 genes associated with very high P-glycoprotein-mediated multidrug transport, resistant to the inhibitory activity of chemosensitizers like verapamil. The physiological modulators of multidrug transport are as yet unknown. We therefore initiated a screening program to analyze the effects of cytokines on multidrug transport. We observed, that transforming growth factors β1, -β2, and β1.2-but not the related bone morphogenetic protein (BMP) 2-inhibited multidrug transport. Interestingly, BMP 2 antagonized the TGF-β induced inhibition of multidrug transport.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00296374
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  • 5
    Electronic Resource
    Electronic Resource
    Long-term expression of heme oxygenase-1 (HO-1, HSP-32) following focal cerebral infarctions and traumatic brain injury in humans (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 377-384 
    Details
    ISSN: 1432-0533
    Keywords: Key words Heme oxygenase-1 ; Heat shock protein-32 ; Traumatic brain injury ; Cerebral infarction ; Immunohistochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Extracellular heme derived from hemoglobin following hemorrhage or released from dying cells induces the expression of heme oxygenase-1 (HO-1, HSP-32) which metabolizes heme to the gaseous mediator carbon monoxide (CO), iron (Fe) and biliverdin. Biliverdin and its product bilirubin are powerful antioxidants. Thus, expression of HO-1 is considered to be a protective mechanism against oxidative stress and has been described in microglia, astrocytes and neurons following distinct experimental models of pathological alterations to the brain such as subarachnoidal hemorrhage, ischemia and traumatic brain injury (TBI) and in human neurodegenerative diseases. We have now analyzed the expression of HO-1 in human brains following TBI (n = 28; survival times: few minutes up to 6 months) and focal cerebral infarctions (FCI; n = 17; survival time: 〈 1 day up to months) by ¶immunohistochemistry. Follwing TBI, accumulation of ¶HO-1+ microglia/macrophages at the hemorrhagic lesion was detected as early as 6 h post trauma and was still pronounced after 6 months. In contrast, after FCI HO-1+ microglia/macrophages accumulated within focal hemorrhages only and were absent in non-hemorrhagic regions. Further, HO-1 was weakly expressed in astrocytes in the perifocal penumbra. In contrast to experimental data derived from rat focal ischemia, these results indicate a prolonged HO-1 expression in humans after brain injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010000202
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  • 6
    Electronic Resource
    Electronic Resource
    Murine monoklonale Antikörper gegen Vibrio anguillarum vom Serotyp I und II (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of applied ichthyology 1 (1985), S. 0 
    Details
    ISSN: 1439-0426
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
    Notes: Murine monoclonal antibodies against Vibrio anguillarum serotype I und IIFour stabil hybridoma cell lines against the Vibrio anguillarum strain 820/15/8 Kopenhagen—a typical serotype I strain—were raised.Three hybridoma cell lines producing monoclonal antibodies against the Vibrio anguillarum strain 134/82/1 Kiel (Serotype II) were established.The specifity of the antibodies was screened by ELISA. Monoclonal antibodies reacted with the characteristic determinant of the respective serotype only.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1439-0426.1985.tb00418.x
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of autoantigen and dexamethasone treatment on expression of endothelial-monocyte activating polypeptide II and allograft-inflammatory factor-1 by activated macrophages and microglial cells in lesions of experimental autoimmune encephalomyelitis, neuritis and uveitis (1999)
    Springer
    Acta neuropathologica 97 (1999), S. 119-126 
    Details
    ISSN: 1432-0533
    Keywords: Key words Leukocyte ; Cytokine ; Inflammation ; Corticosteroids ; Nervous system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Endothelial-monocyte activating polypeptide II (EMAP II) and allograft-inflammatory factor-1 (AIF-1) are two proteins produced by activated monocytes and microglial cells. We now report expression of these factors during experimental therapy of rat neuroautoimmune diseases. Comparative analysis of two therapeutic strategies, treatment with high doses of recombinant autoantigens or with dexamethasone, revealed unexpected differences. High doses of autoantigen were most effective in experimental autoimmune encephalomyelitis and neuritis (EAE and EAN), but less effective in experimental autoimmune uveitis (EAU). Low and high doses of dexamethasone treatment greatly reduced the severity of EAE, EAN and EAU at day 11, but a relapse was observed between days 21 and 26. Only rather limited expression of EMAP II and AIF-1 is seen in the normal central nervous system (CNS). This constitutive expression is not abolished by dexamethasone treatment. In inflammatory autoimmune lesions of the rat CNS, prominent AIF-1 and EMAP II staining was seen with macrophages and monocytes. In particular, parenchymal microglial cells were now activated to express AIF-1 and EMAP II. In accordance with prevention of neurological signs, histological observations revealed that accumulation of activated monocytes expressing EMAP II and AIF-1 in the CNS or peripheral nervous system and the massive expression of these factors by parenchymal microglial cells is inhibited by high doses of autoantigen. Dexamethasone prevented or abolished local expression of EMAP II and AIF-1 at days 10–16. However, an acute and severe relapse occurred in encephalomyelitis between days 20–26. In these cases, a smoldering expression of EMAP II and AIF-1 persisting long after cessation of neurological signs was observed. Thus, expression of EMAP II and AIF-1 by infiltrating activated macrophages is a marker of disease activity and expression of these factors could be used to demonstrate ‘silent’ lesions in the CNS and prolonged microglial cell activation. Apparently, AIF-1 and EMAP II immunoreactivity are tools to stage activation of monocytes and microglial cells in inflammatory lesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050964
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  • 8
    Electronic Resource
    Electronic Resource
    Widespread expression of MRP8 and MRP14 in human cerebral malaria by microglial cells (1998)
    Springer
    Acta neuropathologica 96 (1998), S. 575-580 
    Details
    ISSN: 1432-0533
    Keywords: Key words Cerebral malaria ; S-100 ; Myeloid-related protein 8 ; Microglia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Human cerebral malaria (CM) is an often fatal infection. The cascades of signaling events resulting in tissue trauma and coma are only slowly becoming unraveled. Here we report that microglial cells – sensitive cellular sensors of threats to the central nervous system – in CM express the myeloid-related proteins MRP8 (S100A8) and MRP14 (S100A9), Ca2+-binding sensor proteins of activated monocytes. Surprisingly, microglial activation was widespread throughout the brain in white and gray matter and not limited to areas of petechial bleedings or sequestration of infected erythrocytes. Further, apoptosis/necrosis is prominent in CM; not only leukocytes appeared apoptotic, neurons also appeared damaged and DNA fragmentation was revealed by in situ nick translation. Thus, a prominent feature of human CM is activation of microglia, and analysis of these reactive microglia might further promote our understanding of CM pathology and guide development of future therapeutic intervention of the local reactive processes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050938
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