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Biomedical subjects

K Kristensson

Publications and source records attributed to K Kristensson.

At least 181 records · Page 10Linked to original sources
PubMed1984

IgM and IgG responses during chronic relapsing experimental allergic encephalomyelitis (r-EAE).

During chronic relapsing experimental allergic encephalomyelitis (r-EAE) in guinea pigs, serum IgM and IgG concentrations increased markedly early in disease. Serum IgM and IgG increased similarly in control animals immunized with Freund's incomplete adjuvant (FIA) and Mycobacterium tuberculosis (MT). In the chronic phase of r-EAE but not in control animals, elevated IgM was also found in central nervous system (CNS) extracts, suggesting intrathecal IgM synthesis. IgG antibodies against myelin and myelin basic protein (MBP) were regularly detected in r-EAE sera from day 21 post inoculation (p.i.), reaching maximum levels in the early chronic phase. IgG antibodies against galactocerebroside (GC) and galactose appeared in some r-EAE sera. Oligoclonal IgG bands were demonstrated in all r-EAE guinea pig sera 21-26 days p.i. The bands in serum decreased in number and strength in the chronic phase. They could be traced to antibodies against MT in 4 of 10 animals, but not to antibodies against myelin, MBP, GC or galactose. Oligoclonal IgG bands were also regularly visualized in r-EAE CNS 124 days p.i., suggesting persistent intrathecal IgG synthesis. They varied in number and migration between different regions of individual CNS. Oligoclonal CNS IgG was related to antibodies against MT in only one of 7 animals, and in no case to antibodies against myelin.

Animals↗
PubMed1984

Mumps virus infection of the developing mouse brain--appearance of structural virus proteins demonstrated with monoclonal antibodies.

Newborn mice and hamsters were inoculated intracerebrally with mumps virus strains of high and low neurovirulence, Kilham and RW, respectively and with an egg-adapted patient isolate. The presence of viral antigen in brain tissue was analyzed with the immunofluorescence technique employing monoclonal antibodies against nucleoprotein (NP), polymerase (P), matrix (M), hemagglutinin-neuraminidase (HN) and fusion (F) mumps virus components. As expected, hamsters developed a fatal encephalitis eight to nine days after infection with the Kilham strain and synthesis of all five structural viral antigens was identified. In contrast, mice infected with any of the virus strains did not develop signs of disease, but in brain material collected on days nine and 12 after infection viral antigen was present in many neurons. However, only NP and P antigens were demonstrable and no infectious virus was present. The antibody response in mice developed later than in hamsters. Neurons in the mouse brain may exert a host cell restriction on the virus maturation, and mice offer a suitable host for the establishment of defective, persistent mumps virus infections.

Animals↗
PubMed1984

Uptake and transport of herpes simplex virus in neurites of rat dorsal root ganglia cells in culture.

Attachment and neuritic transport of herpes simplex virus (HSV) type 1 (McIntyre) were studied in a cell culture system with dissociated cells of rat dorsal root ganglia. The two-chamber cell culture system containing a diffusion barrier penetrated by neurites of cultured sensory neurons permitted infection of neurites extending outside the diffusion barrier without exposure of the neuronal cell soma. HSV adsorbed to neuritic extensions and reached the neuronal soma within 1.5 h post-inoculation. Neuritic uptake and transport of HSV were inhibited in the presence of cytochalasin B. Internalization of virus in neurites was preceded by attachment of virus to the neurite plasma membrane. Neurites transported viral nucleocapsids (NC) through the diffusion barrier of the cultures. Destruction of the neuritic extensions before or shortly after peripheral virus inoculation blocked spread of infection to the cell soma. No infection was established when neuritic extensions were exposed to viral NC and NC were then not observed inside the neurite plasma membrane. Virus produced in neurons, when HSV was inoculated into the inner culture chamber containing the neuronal cell bodies, was transported as enveloped virus in cytoplasmic vesicles from the neuronal cell body towards the periphery. Schwann cells were infected by viropexis. Shortly after infection virions were observed in vacuoles of the cytoplasm.

Animals↗
PubMed1983

Herpes simplex virus-induced demyelination. Effects of reinfection and challenge with neuroantigens.

Mice injected into the snout with the F-strain of herpes simplex virus (HSV) showed demyelination in the central part of the trigeminal root and brainstem. In this well characterized model the effect of reinfection with a virulent strain of HSV, and of immunization with UV-light-inactivated HSV and neuroantigens were examined. A marked enhancement of demyelination was found in mice immunized with spinal cord extracts in Freund's adjuvant prior to the HSV infection. Whether this effect is mediated by a general stimulation of inflammatory or immune competent cells or is dependent upon exposure to specific antigens is not known.

Animals↗
PubMed1983

Sendai virus infection in the brains of mice: distribution of viral antigens studied with monoclonal antibodies.

Newborn and 12- and 21-day-old mice were inoculated intracerebrally with Sendai virus. Titers of infectious virus peaked on days 1-2 after infection and had disappeared after three days in 12- and 21-day-old mice and six days in newborn mice. The levels of infectious virus in the brain declined before the appearance of serum antibodies, which in newborn mice was delayed until day 12. Immunofluorescence analysis showed viral antigens in neurons and their dendritic processes 12 and 24 days after infection in newborn animals but not in older ones. Immunofluorescent staining with monoclonal antibodies to five major structural components of Sendai virus--the nucleocapsid, polymerase, matrix, fusion, and hemagglutinin-neuraminidase proteins--showed that all were present in choroid plexus epithelial cells and ependymal cells during acute infection. However, during acute and persistent infections in neurons, the first three antigens were found, but the last two--surface glycoproteins--were lacking or found at low levels.

Animals↗
PubMed1983

Cellular localization of five structural proteins of Sendai virus studied with peroxidase-labelled Fab fragments of monoclonal antibodies.

By the use of horseradish peroxidase-labelled Fab fragments of monoclonal antibodies, five major structural components of Sendai virus, namely the nucleocapsid (NP), polymerase (P), matrix (M), fusion (F), and haemagglutinin-neuraminidase (HN) proteins were localized in infected Vero cells. The P and NP proteins were found in association with large clusters of ribosome-like particles and nucleocapsids in the cell cytoplasm. They were not concentrated at the cytoplasmic membrane, except in nucleocapsids within budding viral particles. F and HN proteins, on the other hand, were found in connection with ribosomes and endoplasmic reticulum in the cell cytoplasm, but not in nucleocapsids. Both proteins were evenly distributed on the outer cytoplasmic membrane and appeared on the surface clearly before budding of viral particles. The M protein was seen in connection with both nucleocapsids and ribosomes. It was not found at the cell surface except in budding viral particles.

Animals↗
PubMed1982

The effect of cytochalasin D and monensin on enveloped vaccinia virus release.

Both monensin and cytochalasin D reduced the production of infectious cell associated virus and infectious extracellular virus with the latter clearly being the more sensitive. The difference in yields were even more clearly seen if the yield of virus particles was monitored instead of yield of infectious virus. Addition of 1 microgram/ml cytochalasin D or 1 microM monensin to the growth medium of vaccinia virus-infected cells inhibited the appearance of extracellular enveloped vaccinia virus (EEV) in the growth medium without affecting the production of intracellular naked vaccinia virus (INV) particles. Although EEV was not released into the medium of cytochalasin D treated cells, EEV was, nevertheless, detectable in CsCl gradients of cell associated virus. Monensin treatment did not affect the synthesis of vaccinia glycoproteins but did significantly reduce the transport of these glycoproteins to the cell surface and also reduced the secretion of proteins. Monensin had the additional effect of causing the appearance of numerous large vacuoles in the cytoplasm. Vaccinia is normally wrapped by cytoplasmic membranes in preparation for release. The monensin induced conversion of cytoplasmic membranes to large vacuoles is presumably the basis for the block in virus wrapping and subsequent release. Cytochalasin D did not alter any of the steps in protein synthesis, transport or secretion. Electronmicroscopic studies confirmed the existence of EEV on the surface of infected cells treated with cytochalasin D. This drug which specifically affects cellular microfilament organisation thus imposes a block on the final release of EEV from the cell surface.

Animals↗
PubMed1982

Virus-induced demyelination in herpes simplex virus-infected mice.

Herpes simplex virus (HSV) infection of the mouse trigeminal ganglia and the brain stem is associated with demyelination of axons in the central part of the trigeminal root and inflammatory cell infiltration and perivascular demyelination in the brain stem. Cyclophosphamide (CPA) treatment prior to or soon after HSV inoculation caused increased axonal spread of infective virus from the peripheral site of inoculation, more widespread and severe demyelination and increased mortality, suggesting that by CPA the virus invasion of the CNS was facilitated. A direct cytocidal effect of HSV on myelinating cells seemed one plausible explanation for the demyelination. Influence on demyelination at late stages of infection by cytotoxic immune reactions are not excluded by the results reported but seemed not to dominate the picture. Schwann cells from the peripheral part of the nerve root invaded demyelinated areas in the brain stem and remyelinated the axons.

Animals↗
PubMed1982

Demonstration of serum IgG antibodies against myelin during the course of relapsing experimental allergic encephalomyelitis in guinea pigs.

Chronic relapsing allergic encephalomyelitis (r-EAE) was induced in a local strain of guinea pigs. By the use of isoelectric focusing (IF) followed by antigen immunofixation and autoradiography, antibodies directed against central nervous system (CNS) myelin were detected in 21 of 23 sera sampled during the course of r-EAE. Previous absorption of the sera with CNS myelin reduced or abolished antibody activity on autoradiograms. One r-EAE guinea pig developed definite oligoclonal IgG bands in serum while in 7 r-EAE animals faint oligoclonal IgG bands were present. The mobility of oligoclonal IgG bands differed from the mobility of antimyelin antibody bands on autoradiograms. The significance of these findings has not been definitely elucidated but the antimyelin antibodies may possibly be involved in the pathogenesis of the disease while oligoclonal IgG bands may represent an epiphenomenon not pathogenetically related to r-EAE.

Animals↗
PubMed1982

Neuron to neuron transmission of herpes simplex virus. Transport of virus from skin to brainstem nuclei.

Herpes simplex virus (HSV) injection into the snout of mice was followed by the appearance of HSV antigen in neurons in trigeminal ganglia, main sensory and spinal tract trigeminal nuclei, reticular formation including raphe nuclei and locus ceruleus on both sides. The findings indicate that HSV spreads via axons, passes through a series of neurons and in this way can reach vital nuclei in the brainstem including monoaminergic neurons from the primary replication area in the lip.

Animals↗
PubMed1982

Neuroaxonal dystrophy in childhood. Report of two second cousins with Hallerworden-Spatz disease, and a case of Seitelberger's disease.

Three late infantile cases of neuroaxonal dystrophy are presented, two of them second cousins with Hallerworden-Spatz disease and one sporadic case with Seitelberger's disease. At about 1 1/2 years of age the patients with Hallerworden-Spatz disease developed clinical signs including progressive extrapyramidal motor disorder and mental retardation. They died at 8 and 11 years. Iron deposits and axonal dystrophy were found in the pallidum. The changes are compared to those in a case of infantile neuroaxonal dystrophy (Seitelberger's disease), the first to be reported in Scandinavia.

Basal Ganglia Diseases↗
PubMed1982

Effect of glycosylation inhibitors on the release of enveloped vaccinia virus.

Addition of 1 to 10 mM 2-deoxy-D-glucose (2-dg) or glucosamine (gln) to the growth medium of vaccinia virus-infected cells inhibited the release of extracellular enveloped vaccinia virus (EEV) without affecting the production of intracellular naked vaccinia virus (INV) particles. In contrast, INV infectivity (particles per PFU) was decreased sevenfold by 50 mM 2-dg. Treatment with 2-dg reduced but did not eliminate glycosylation of the INV 37,000-molecular-weight glycoprotein. The kinetics of sensitivity to inhibitor addition experiments and inhibitor reversal experiments indicated that EEV release was dependent on glycosylation before 8 h postinfection. This was supported by polyacrylamide gel electrophoretic analysis of the synthesis kinetics for cell membrane-associated vaccinia glycoproteins in 2-dg-inhibited infected cells. The dependence of vaccinia protein glycosylation before 8 h postinfection for efficient EEV release was observed in spite of the fact that the period of greatest glycoprotein synthesis was 8 to 12 h postinfection. The presence of 2-dg resulted in an incompletely glycosylated 89,000-molecular-weight glycoprotein, as indicated by a reduction in the apparent glycoprotein molecular weight. The morphological event affected by the inhibitors was the acquisition by INV of a double-membrane structure from the Golgi apparatus. This morphological intermediate is necessary for release of EEV.

Animals↗
PubMed1981

Somatopetal axonal transport of fluorescent lectins: distribution pattern and cytophotometric quantification in mouse peripheral neurons.

Six FITC-labeled lectins (Con A, WGA, SBA, DBA, UeA 1, PNA) with different carbohydrate specificities were injected into the snout region of 12-day-old mice. WGA, and to a lesser extent Con A, accumulated in trigeminal and facial neurons as a result of somatopetal axonal transport. Only an occasional trigeminal neuron was labeled after injection of SBA and DBA. None of the other lectins were incorporated. WGA and Con A were used for cytophotometric quantification of neuronal accumulation of transported FITC-lectins in isolated neurons from trigeminal ganglia. This technique makes it possible to study changes in neuronal lectin binding sites and adsorptive endocytosis during different physiological and pathological states.

Animals↗
PubMed1981

Toxicity and neuronal transport of stable liposomes and phospholipid in the nervous system.

When unilamellar "stable" liposomes composed of a dialkyl analog of phosphatidylcholine, tetradecyloctadec-11-eno(1)phosphocholine (dialkyl-PC), plus cholesterol at 1:1 molar ratio, and a trace of [3H]dialkyl-PC were injected into the vitreous of the rabbit eye, macrophage infiltration and phagocytosis of lipid were observed in retina including the epiretinal myelinated nerve fiber bundles, with no other neurotoxic effects. Little or no incorporation of [3h]dialkyl-PC was observed in the distal tissues of the optic system. With "labile" vesicles composed of egg lecithin, trace amounts of [3H]dialkyl-PC, and phosphatidic acid, no morphological changes occurred. After a lag of more than 7 days [3H]dialkyl-PC appeared in superior colliculus, indicating axonal transport of the lipid in an anterograde direction. Experiments with submandibular and parotid gland indicated retrograde transport of the lipid. The data do not suggest axonal transport of intact (stable) liposomes, but suggest that intact phospholipid molecules can be axonally transported.

Afferent Pathways↗
PubMed1981

Myelinotoxic activity on tadpole optic nerve of IgG isolated from CSF and serum of patients with multiple sclerosis.

IgG from individual cerebrospinal fluid (CSF) and sera from patients with multiple sclerosis and from controls was isolated by protein A-Sepharose column chromatography and tested in the tadpole optic nerve system for myelinotoxic activity. Oligoclonal IgG was present in all multiple sclerosis CSF specimens used. All IgG preparations yielded optic nerve myelin lesions, indicating that IgG has myelinotoxic activity. Significantly higher numbers of myelin lesions were obtained with IgG prepared from multiple sclerosis CSF compared to control CSF IgG.

Adult↗