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Biomedical subjects

M Vandevelde

Publications and source records attributed to M Vandevelde.

At least 91 records · Page 5Linked to original sources
PubMed1989

Antiviral antibodies stimulate production of reactive oxygen species in cultured canine brain cells infected with canine distemper virus.

Canine distemper is characterized mainly by respiratory, enteric, and nervous symptoms. Infection of the central nervous system results in demyelination, to which inflammation has been shown to contribute significantly. It has been proposed that macrophages play a major role as effector cells in this process. We report that cultured dog brain cells contain a population of macrophages capable of producing reactive oxygen species as measured by luminol-dependent chemiluminescence. In cultures infected with canine distemper virus, a burst of reactive oxygen is triggered by antiviral antibody. This response depends on the presence of viral antigens on the surfaces of infected cells and is mediated by the interaction of antigen-bound antibody with Fc receptors on the macrophages. Since there is no evidence in vitro or in vivo that oligodendrocytes, the cells forming myelin, are infected, our observation supports the hypothesis that "innocent bystander killing" is important in demyelination caused by canine distemper virus. Reactive oxygen species released from macrophages may contribute to destruction of myelin.

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PubMed1989

[Macrophages in central nervous canine distemper: friends or foes?].

Brain macrophages play an important role in the CNS. We review some biological aspects of brain macrophages in vivo and in vitro. The criteria and methods used for the identification of these cells are considered. They include some morphological features such as the use of histochemical and immunocytochemical techniques for internal and surface components. In the second part of this review, we describe the role of brain macrophages in canine distemper encephalitis as proposed earlier by us. Studies in cultured dog glial cells infected with canine distemper virus (CDV) have shown that brain macrophages stimulated by anti-CDV antibodies will release reactive oxygen species as measured by chemiluminescence. This response depends on the presence of viral antigens on the surfaces of infected cells and is mediated by the interaction of antigen-bound antibodies with Fc receptors on brain macrophages. These observations support the hypotheses that brain macrophages may contribute to the damage of the white matter observed in canine distemper encephalitis.

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PubMed1989

[Diagnostic aspects of neurological diseases of cattle. A retrospective study].

188 bovines with neurological disease were analysed in a retrospective study. We found that only few diseases can be diagnosed on the basis of neurologic signs only. However, with a few additional clinical data such as signalment, history, extraneural findings, hematological findings and cerebrospinal fluid analysis, a diagnosis can be made in many cases. A history of neurologic signs occurring since birth, is highly suggestive of a congenital malformation. High fever and mucosal changes are typical for malignant catarrhal fever. Lesions of peripheral nerves and spinal cord compression can be diagnosed based on the neurologic signs. Cranial nerve dysfunction and central vestibular signs in combination with other findings as age, season and cerebrospinal fluid, are indicative of listeriosis. Tetanus is characterized by pronounced extensor rigidity. Systemic muscle diseases were also included, because motor neurons and muscle cells are a functional unit. A suspicion of white muscle disease can be confirmed by increased creatine phosphokinase activity in serum. Suppurative bacterial meningoencephalitis can be diagnosed by the presence of a polymorphonuclear pleocytosis in the cerebrospinal fluid. The clinical differentiation between sporadic non suppurative meningoencephalitis and metabolic diseases of the central nervous system remains difficult.

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PubMed1988

Transferrin, carbonic anhydrase C and ferritin in dissociated murine brain cell cultures.

It is shown here that transferrin (Tf), the iron transport protein and carbonic anhydrase C (CA C) are specifically located within oligodendrocytes in murine brain cell cultures. Ferritin (F), the major iron storage protein, was demonstrated in oligodendrocytes, as well as in astrocytes and microglial cells and was more prominent in the former. CA C and Tf were seen first after 6-7 days in culture. CA C and F positivity increased rapidly and at day 20, 80-85% of galactocerebroside + oligodendrocytes were positive for both proteins. Only a small number of oligodendrocytes was Tf+ up to day 14, after which their numbers increased rapidly until day 20, when 67% of the oligodendrocytes were Tf+. Because of the presence of Tf and F in oligodendrocytes it is suggested that these cells may play an important role in the metabolism of iron within the central nervous system.

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PubMed1987

Oligodendroglial pathology in canine distemper virus infection in vitro.

Dog brain cell cultures were infected with different canine distemper virus (CDV) strains to study the oligodendrocytes, which were characterized with eight different antibodies to cover the whole oligodendroglial population in the culture. A few weeks after infection all oligodendroglial cell types started to degenerate and disappeared from the culture. However, since no CDV protein could be demonstrated in the degenerating oligodendrocytes with extensive double-labelling studies, this lesion can not be explained as being a result of cytolytic infection. This conclusion was further supported in experiments with plaque-forming CDV, in which viral replication is restricted to the cytolytic areas only; oligodendrocytes also degenerated in virus-free areas between the plaques. The hypothesis of toxic factors released by other infected cell types in the culture leading to secondary damage of the oligodendrocyte could not be confirmed by transferring supernatants from infected to normal cultures. Whereas the presence of toxic factors can not be completely excluded, the possibility of an abortive infection of the oligodendrocytes with no or very limited viral protein synthesis is discussed.

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PubMed1987

Demyelinating, non-demyelinating and attenuated canine distemper virus strains induce oligodendroglial cytolysis in vitro.

A virulent canine distemper virus (CDV) strain that causes demyelination in vivo has been shown to induce oligodendroglial degeneration in vitro. In order to investigate if this effect on oligodendrocytes is specific for demyelinating strains only, primary brain cell cultures were infected with either virulent demyelinating strains (A75/17 and CH84-CDV), a virulent non-demyelinating strain (SH-CDV) or a non-virulent strain (OP-CDV). All virulent viruses caused a persistent type infection with moderate cytolysis whereas the non-virulent strain was highly cytolytic. All strains induced a similar pattern of oligodendroglial degeneration. It was concluded that the ability to induce oligodendroglial degeneration, which is thought to be the in vitro correlate of demyelination in vivo, is inherent to CDV irrespective of the strain. The discrepancy between biological behaviour of CDV strains in brain cell cultures and in vivo can be explained by the more complex virus-cell interactions in vivo than in vitro.

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PubMed1986

Canine distemper virus clearance in chronic inflammatory demyelination.

The distribution of canine distemper virus (CDV) antigen was examined in the brains of 14 dogs with chronic nervous distemper using a monoclonal antibody against a major viral protein. In ten of these dogs, neutralizing anti-CDV antibody titers were determined in serum and unconcentrated cerebrospinal fluid (CSF). In 19% of the inflammatory demyelinating lesions, large amounts of CDV antigen were found; in 34% of these lesions only residual traces of virus were seen and in almost half of the lesions (47%) no CDV could be demonstrated. In four dogs neutralizing antibodies were found in the serum only; in one dog in the CSF only and in 5 dogs both in serum and CSF. Because of the correlation between the presence of inflammation, intrathecal antiviral antibodies and disappearance of CDV from the lesions, it was concluded that the inflammatory response in distemper is associated with viral clearance from the lesions. Associated immune-mediated cytotoxic reactions could explain exacerbation of the initial virus-induced demyelinating lesions. Despite the presence of an apparently effective intrathecal antiviral immune response, fresh non-inflammatory lesions as a result of viral replication and spread in the white matter coexisted with inflammatory ones in which viral clearance had taken place. The role and mechanism of such virus persistence are discussed.

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PubMed1986

Studies on the intrathecal humoral immune response in canine distemper encephalitis.

Albumin and IgG were quantitated in paired cerebrospinal fluid (CSF) and serum samples from dogs with demyelinating canine distemper virus (CDV) infection by means of rocket immunoelectrophoresis. The IgG index as indicator for intrathecal immunoglobulin synthesis was normal in animals with non-inflammatory demyelinating lesions and elevated in dogs with inflammatory myelin lesions. Specific antibodies against CDV and myelin were quantitated in CSF and serum from 8 dogs with an elevated IgG index. Eight of these dogs had significant amounts of antimyelin antibody and 4 dogs had neutralizing anti-CDV antibody in the CSF. Whereas the pathogenetic significance of antimyelin antibodies remains uncertain, the intrathecal antiviral immune response provides a plausible explanation for immunopathologic destruction of myelin in distemper.

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PubMed1986

Secondary degeneration of oligodendrocytes in canine distemper virus infection in vitro.

To study the pathogenesis of demyelination in canine distemper virus (CDV) infection, primary canine brain cell cultures were infected with CDV to examine specific virus-induced glial cell changes. Cultures were harvested at regular intervals after inoculation and were immunostained for the specific demonstration of astrocytes, oligodendrocytes, and CDV antigen. The infection spread slowly with moderate cytolysis and cell fusion. Soon after inoculation, infection of astrocytes was found by means of double immunofluorescent labeling. One week after inoculation, CDV-induced astrocytic fusion and rearrangement of astroglial fibrils became apparent. The astrocytic changes progressed during the observation period. Double immunofluorescent labeling failed to show oligodendroglial infection. Despite clear absence of viral replication within oligodendrocytes at all stages of the experiment, these cells exhibited marked pathologic changes starting at about 20 days after inoculation and progressed to complete cytolysis within 10 days. The degeneration of the oligodendrocytes was thought to be secondary to CDV-induced changes in other cell types of the culture probably through the release of toxic factors in the tissue culture medium. Since little evidence has been found for oligodendroglial infection in demyelinating lesions in canine distemper in vivo, the present tissue culture findings suggest that demyelination in vivo could be the result of indirect oligodendroglial damage caused by CDV-induced changes in other cell types such as astrocytes.

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PubMed1985

Spread and distribution of viral antigen in nervous canine distemper.

Canine distemper virus (CDV) antigen was demonstrated immunocytochemically in the central nervous system (CNS) of 19 dogs killed from 16 to 170 days after infection. In the earliest lesions, infection of glial cells preceded demyelination, and the degree of myelin destruction correlated with the amount of viral antigen in the tissue. It was concluded that initial demyelination in distemper is directly viral-induced, but the nature of the infected glial cells remains uncertain. Ependymal infection and spread of virus in the subependymal white matter was often seen, suggesting invasion of CDV into the CNS along the CSF pathways. Inflammation during the latter stages of the infection appeared to be associated with viral clearance from the CNS in most dogs. In two dogs with chronic progressive neurologic distemper, viral antigen was still present in the brain suggesting that viral persistence and associated immunologic reactions may contribute to further myelin damage. With the exception of one dog that survived for 6 months after infection, viral antigen was no longer detected in the dogs that had recovered.

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PubMed1985

Immunocytochemical studies in canine neuroectodermal brain tumors.

Seventy-four canine neuroectodermal tumors were examined immunocytochemically for the presence of glial fibrillary acidic protein (GFAP). Eleven oligodendrogliomas were examined for the presence of myelin basic protein (MBP) and myelin-associated glycoprotein (MAG). Twenty-three tumors, including ten astrocytomas, one ependymoma, two glioblastomas, one case of gliomatosis, and nine poorly differentiated gliomas were positive for GFAP. Two astrocytomas, eleven oligodendrogliomas, eight ependymomas, four choroid plexus papillomas, two medulloblastomas, one glioblastoma, nine poorly differentiated gliomas, six cases of gliomatosis, and three unclassified tumors were GFAP-negative. In six tumors (including four that were classified as astrocytoma) GFAP staining was equivocal. All oligodendrogliomas were MBP-negative but three expressed MAG. It was concluded that many canine gliomas are not only morphologically but also immunocytochemically similar to human gliomas, but that a larger proportion of canine neuroectodermal growths are undifferentiated tumors.

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PubMed1985

Canine distemper virus does not infect oligodendrocytes in vitro.

Dissociated canine brain cell cultures were infected with virulent canine distemper virus (CDV). Double immunofluorescent labelling was done to simultaneously demonstrate viral antigen and specific glial cell markers. Virus containing oligodendrocytes were not found at any stage of the infection. A certain proportion of the infected cells were shown to be astrocytes. It was concluded that CDV has no obvious tropism for oligodendrocytes which could explain the mechanism of demyelination in distemper in vivo.

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PubMed1985

A monoclonal antibody that binds to both astrocytes and myelin sheaths.

A monoclonal antibody designated III 5H8 was shown to bind both to astrocytes and to myelin sheaths as studied with immunocytochemical techniques on brain sections and cell cultures. Binding to astrocytes was confirmed by double immunofluorescent labelling of frozen sections and cell cultures with anti-GFAP, and appeared to be sensitive to formalin treatment. Binding to myelin sheaths was confirmed by comparing sections labelled with III 5H8 with sections labelled with antibodies against axons and myelin basic protein as well as by staining of sections of hypomyelinated spinal cord with III 5H8. On immunoblots of separated white matter III 5H8 revealed two bands, while on immunoblots of purified myelin only one band was seen. The findings are discussed with respect to the function of astrocytes in white matter and shared antigenic determinants between astrocytes and oligodendrocytes.

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