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Biomedical subjects

U Traugott

Publications and source records attributed to U Traugott.

At least 37 records · Page 2Linked to original sources
PubMed1985

Acute experimental allergic encephalomyelitis in the mouse: immunopathology of the developing lesion.

To investigate the sequence of immunopathologic events during lesion formation in acute experimental allergic encephalomyelitis (EAE), SJL/J mice were inoculated with isogeneic spinal cord in complete Freund's adjuvant (CFA) and with Bordetella pertussis on Days 1 and 3 postinoculation (PI). Mice were sampled at different time points PI and T cells, T-cell subsets. Ia+ cells, Ig+ cells, albumin, and Ig deposits were localized in frozen sections by the avidin-biotin complex (ABC) method and direct fluorescence. Furthermore, samples were stained for Ia antigen, myelin basic protein (MBP), and galactocerebroside (GC) localization on endothelial cells by the ABC technique. Clinical and pathologic observations were correlated with the immunopathologic results. It was found that early in the disease process myelin and Ia-antigens were demonstrable on endothelial cells within the central nervous system (CNS). Simultaneously, damage to the blood-brain barrier was apparent, as indicated by albumin deposits, and small numbers of infiltrating T cells, T-cell subsets, and Ia+ cells were found. With time PI, the density of infiltrating total T cells (Thy-1.2+), helper/inducer (Lyt-1+), and suppressor/cytotoxic (Lyt-2+) T cells increased; Lyt-1+ and Lyt-2+ cells were detectable in meningeal as well as parenchymal infiltrates, while later on, Lyt-1+ cells showed some predilection for the CNS parenchyma and Lyt-2+ cells for meninges. Ia+ cells (B cells, macrophages, activated T cells) were present in small numbers only. Ig+ cells (B cells and macrophages) appeared shortly before onset of signs and persisted in moderate numbers. These results reconfirm the importance of early T-cell involvement for the development of EAE; they might also indicate a secondary role for Ig+ cells and are consistent with the concept that presentation of myelin antigens to T cells might occur locally on Ia-bearing endothelial cells within the CNS.

Acute Disease↗
PubMed1985

Dose-dependency of MBP-induced demyelination in the guinea pig.

The pathology of experimental allergic encephalomyelitis (EAE) induced by bovine myelin basic protein (MBP) has been examined in the guinea pig with a series of doses ranging from 37.5 micrograms to 600 micrograms. This was to investigate whether the previously demonstrated lack of demyelinative effect by MBP was dose-related. At all doses tested, MBP induced clinical disease. Inflammation was the major feature of lesions in all animals. However, no demyelination was seen when 75 micrograms MBP or less was given. At higher doses (150 micrograms upwards), MBP always induced intense inflammation but demyelination was encountered inconsistently. These observations support the contention that in addition to an immune response to MBP, other factors contribute to autoimmune demyelination.

Animals↗
PubMed1985

Multiple sclerosis. Evidence for antigen presentation in situ by endothelial cells and astrocytes.

To investigate the possibility of local antigen presentation within the central nervous system (CNS) in multiple sclerosis (MS), frozen sections of active chronic MS lesions were stained by the peroxidase-antiperoxidase technique for the demonstration of Ia antigen using a monoclonal antibody. Ia antigen could be localized on some endothelial cells and astrocytes as well as on macrophages. While Ia+ endothelial cells were randomly distributed throughout the CNS, Ia+ astrocytes were mainly found at the edge of active chronic MS lesions. These findings in MS suggest that antigen might be presented locally within the CNS on endothelial cells, where it might lead to new lesion formation by the initiation of a local immune response; on astrocytes, where it might be involved in lesion growth at the periphery.

Astrocytes↗
PubMed1985

On the presence of Ia-positive endothelial cells and astrocytes in multiple sclerosis lesions and its relevance to antigen presentation.

Using a monoclonal antibody in combination with the 4-step modified peroxidase-antiperoxidase (PAP) technique, Ia expression was demonstrated on endothelial cells and astrocytes in MS lesions of different ages. On endothelial cells, Ia antigen was found most frequently in grey and white matter parenchyma of acute MS brain and showed lower, comparable numbers in active and silent chronic MS brain tissue. Ia+ astrocytes were most numerous in acute MS lesions. In active chronic MS, Ia+ astrocytes predominated at the lesion edge, where they frequently displayed an atypical, rounded configuration. Positive astrocytes showed somewhat lower numbers within the lesion center and in normal white matter close to the lesion edge. Their frequency was significantly lower in normal white matter remote from the lesion. In silent chronic MS, Ia+ astrocyte processes were detectable only within the lesion center. Grey matter astrocytes displayed no staining with anti-Ia antibody. In normal brain tissue, no Ia antigen could be detected. The presence of Ia molecules on some endothelial cells and astrocytes in MS brain tissue suggests a role in antigen presentation perhaps relevant to the initiation and perpetuation, respectively, of the inflammatory process.

Antibodies, Monoclonal↗
PubMed1979

Oligodendrocyte staining by multiple sclerosis serum is nonspecific.

The immunofluorescent staining properties of 65 serum samples from 54 patients with multiple sclerosis (MS), 63 samples from 55 patients with other neurological diseases (OND), and sera from 14 healthy normal individuals were examined on frozen sections of bovine and human brain. When tested on bovine brain sections, positive oligodendrocyte staining was present in 63% of MS sera, 43% of OND sera, and 29% of normal sera. The percentages were lower with human brain tissue. Astrocyte and myelin staining was common. F(ab')2 fragments purified from selected positive and negative MS and control sera gave no staining, though IgG fractions from the same sera prior to pepsin digestion gave positive staining. When tested against antihuman IgM and IgA conjugates, the same positive sera and their IgG-depleted globulin fractions gave minimal or no staining. These results indicate that oligodendrocyte staining is not specific for MS, is not due to specific antibody, and is probably the result of nonspecific binding to Fc receptors.

Animals↗
PubMed1979

Multiple sclerosis: circulating antigen-reactive lymphocytes.

Circulating lymphocyte populations were examined in 85 patients with multiple sclerosis (MS), 26 of whom showed exacerbations; 48 patients with other neurological diseases (OND); 14 patients suffering from psychiatric disorders; and 2 normal subjects. The study involved the assay of early (active, high-affinity rosetting) T-cells, myelin basic protein (MBP)-reactive early T-cells, late (total, 24-hour rosetting) T-cell levels were significantly lower in MS (p less than 0.01) than in OND subjects. Exacerbations in MS were usually accompanied by further decreases in early T-cells. The lower levels of early T-cells in MS and their fluctuations are believed to reflect disease activity. MBP-reactive early T-cells were more frequently increased in MS (75% of cases) than OND (50%), and while this might be indicative of increased sensitization against myelin antigens, it was found not to be an MS-specific phenomenon.

Adult↗
PubMed1979

Experimental allergic encephalomyelitis. Frequent sampling of blood alters disease course.

Previous studies have shown that Strain 13 guinea pigs sensitised for experimental allergic encephalomyelitis (EAE) as adults usually develop an acute, fatal form of disease while animals inoculated as juveniles usually display a chronic relapsing form. The present study reports that following repeated short-interval blood sampling by cardiac puncture for the estimation of lymphocyte populations, some adult Strain 13 guinea pigs sensitised for acute EAE unexpectedly survived and developed chronic EAE, while a group of juveniles sensitised for chronic EAE and bled under the same conditions, developed a more severe, acute form of EAE. It is suggested that this reversal of disease course was related to the depletion of circulating factors.

Age Factors↗
PubMed1979

Chronic relapsing experimental allergic encephalomyelitis. Correlation of circulating lymphocyte fluctuations with disease activity in suppressed and unsuppressed animals.

Groups of juvenile Strain 13 guinea pigs sensitized for chronic relapsing experimental allergic encephalomyelitis (EAE) with isogeneic central nervous system (CNS) tissue in complete Freund's adjuvant (CFA) were either left to develop late-onset chronic EAE (unsuppressed), or given a series of injections of bovine myelin basic protein (MBP) in incomplete Freund's adjuvant (IFA) to suppress the disease. All unsuppressed animals developed disease and all suppressed animals remained healthy over a 27-month period of study. some unsuppressed and suppressed animals were rechallenged with CNS tissue in CFA 12 or 26 months post-inoculation (PI). Unsuppressed animals all became sick 2-4 weeks after rechallenge, while rechallenged, suppressed animals were protected, indicating that the suppression was permanent. Pathologic findings in the CNS complemented the clinical changes. Circulating lymphocyte studies were performed on animals from all groups. Early (active, high-affinity rosetting) T cell levels in unsuppressed animals showed significant decreases during exacerbations (P less than 0.01) and normal values during remissions. After rechallenge, circulating early T cells decreased in unsuppressed animals with the development of signs. In suppressed animals, early T cells showed significant elevations during, and for a short time after, the period of suppressive injections, and normal values afterwards. These levels did not change significantly after rechallenge. Late (total, 24 hour rosetting) T cell and B cell values showed minor fluctuations only which did not correlate with disease activity. These results indicate that chronic relapsing EAE can be successfully suppressed with MBP in IFA, that this suppression is permanent and that the immunologic findings presented correlate well with the clinical and pathologic facets of the disease. the findings are presented in terms of their relevance to multiple sclerosis.

Animals↗
PubMed1979

Acute experimental allergic encephalomyelitis. Myelin basic protein-reactive T cells in the circulation and in meningeal infiltrates.

MBP-reactive early T cells were determined simultaneously in the circulation and in inflammatory cells from the meninges of guinea pigs with acute EAE. In addition, early and late T cells as well as B cells were estimated in both compartments. Within the circulation, early T cells were found to decrease at the onset of clinical signs, and MBP-reactive early T cells were significantly higher than in normals. Different changes were found in inflammatory cells from the meninges. In this cell population, early T cells were increased but did not show significant, further elevation after incubation with MBP. This may indicate that the majority of early T cells in meningeal infiltrates had been previously activated by MBP in vivo.

Acute Disease↗
PubMed1978

T and B lymphocytes in the cerebrospinal fluid of various neurological diseases.

Cerebrospinal fluids (CSF) from 66 patients with a variety of neurological disorders were studied for total protein content, absolute amount of albumin, IgA, IgG and IgM, as well as their quotients (fraction to total protein ratio), cell numbers and B cell and T cell levels. In addition, the percentage of B cells and T cells in the blood was determined in 34 patients and serum immunoglobulin levels were estimated in 51 patients. In noninflammatory diseases of the CNS, the percentage of B cells was slightly higher and T cell levels were lower in the CSF in comparison to corresponding blood values. The B cell to T cell ratio in viral meningitis was altered in the CSF. An apparent increase in the T cell level led to a decrease of B cell values. Similar changes were also found in optic neuritis. The percentage of T cells was higher in relapsing multiple sclerosis than in the chronic progressive form. There were less striking changes in the B cell to T cell ratios in the CSF of other inflammatory diseases of the CNS.

Adolescent↗
PubMed1978

Chronic relapsing experimental allergic encephalomyelitis: CNS plaque development in unsuppressed and suppressed animals.

Central nervous system (CNS) lesion morphology has been studied in inbred Strain 13 guinea pigs sensitized for chronic relapsing EAE in which the disease was either left to develop (unsuppressed) or was suppressed with injections containing myelin basic protein (MBP). Pathologic changes correlated well with clinical activity. In unsuppressed chronic EAE animals, active clinical disease was invariably matched by acute inflammation in the CNS. In more chronic states, the CNS displayed fibrosis and remyelination while relapses showed the CNS to contain recent changes superimposed upon old lesions. In animals in which the disease was suppressed by injections of MBP, clinical signs did not develop. However, some early subclinical changes were seen morphologically. These lesions were able to remyelinate early on and there was no progression in lesion formation. Apparently, therefore, MBP had a beneficial effect upon the course of the disease and had promoted structural repair. It thus appears that MBP therapy might be one effective approach for the prevention of chronic relapsing EAE. The findings should prove relevant to future MBP trials in multiple sclerosis.

Animals↗
PubMed1978

Suppression of chronic allergic encephalomyelitis: relevance to multiple sclerosis.

The expression of chronic relapsing experimental allergic encephalomyelitis in strain 13 guinea pigs was suppressed with a single series of injections of myelin basic protein in incomplete Freund's adjuvant. The suppression appeared permanent, and subsequent rechallenge with central nervous system antigen failed to elicit exacerbations.

Animals↗
PubMed1978

[Tetanus antitoxin in serum and cerebral spinal fluid in viral meningitis in children (author's transl)].

Tetanus antitoxins were measured in serum and cerebro spinal fluid from 58 children--35 boys and 23 girls--with viral meningitis. The concentrations of IgG, IgA and IgM were also determined. The appearance of tetanus antitoxins in cerebral spinal fluid depends on absolute antitoxin levels in serum as well as on the antitoxin/IgG ratio. Antitoxin/IgG ratios in serum and cerebro spinal fluid were in the same order of magnitude. Detection of tetanus antitoxins in the cerebral spinal fluid of children with viral meningitis shows clearly that antibody found in cerebral spinal fluid is not an absolute proof of a certain disease. The results further indicate that local production of IgG antibody cannot be postulated by detecting certain antibodies in the CSF. It is also necessary to prove that antibody/globulin ratios are of significantly different magnitude in serum and CFS.

Adolescent↗
PubMed1978

Encephalitogenic properties of purified preparations of bovine oligodendrocytes tested in guinea pigs.

The present study has investigated central nervous system disease in guinea pigs inoculated with emulsions containing purified preparations of bovine oligodendroglia and their fractions isolated with or without trypsinization, whole bovine white matter or myelin basic protein (MBP). The MBP content of the oligodendroglial fractions was determined by radioimmunoassay. It was found that oligodendroglia prepared from trypsinized fresh brain contained minute amounts of MBP and did not induce disease. The corresponding cell fraction from non-trypsinized frozen brain was rich in MBP and induced disease. Bovine white matter and MBP induced typical experimental allergic encephalomyelitis (EAE). The structural preservation of the non-encephalitogenic trypsinized MBP-poor cells was very good and that of the encephalitogenic MBP-rich non-trypsinized cells very poor. It has been concluded that the encephalitogenicity observed was due to MBP, rather than to a specific oligodendroglial antigen.

Animals↗
PubMed1978

Characterization of antioligodendrocyte serum.

An antioligodendrocyte serum (AOS) has been raised in rabbits against preparations of isolated bovine oligodendrocytes. The antibody was assayed by two techniques. By complement fixation with isolated oligodendrocytes, the titer of the antibody was 1:64 to 1:128. By indirect immunofluorescence testing of oligodendrocyte suspensions and frozen brain sections, the titer of the AOS was 1:256 to 1:512. When unabsorbed AOS was used, immunofluorescent staining proved it specific for bovine oligodendrocytes in suspension and in sections, and for human oligodendrocytes in sections. In cell suspensions, the staining was membrane related and in sections, cytoplasmic. The oligodendrocyte staining could be totally removed by absorption of AOS against oligodendrocyte suspensions, whereas absorption against bovine myelin, bovine myelin basic protein, and bovine neurons did not affect the staining reaction. AOS also stsined Schwann cells, a property possible related to antigens shared with oligodendrocytes. It is concluded that AOS is specific for oligodendrocytes and can now be applied to fundamental and disease-rel

Animals↗
PubMed1978

Glial bridges and Schwann cell migration during chronic demyelination in the C.N.S.

The formation of fibrotic bridges from subpial astrocytes into the subarachnoid space of the spinal cord and the migration of Schwann cells to the central nervous system (C.N.S.) is appraised in chronically demyelinated C.N.S. lesions. Spinal cord tissue was studied from inbred, Strain 13 guinea pigs with chronic experimental allergic encephalomyelitis (EAE). It has been found that uncommitted Schwann cells are present around remyelinated fibres in nerve root entry zones, between meningeal cells at a distance from the roots and along blood vessels within the spinal cord parenchyma. It is speculated that these cells migrate via the above route to the C.N.S. In the present model, this invasion might be aided by glial fibrosis, a process which leads to surface irregularities in the spinal cord, an extensive extracellular space and possible breaches in the glia limitans through which Schwann cells might penetrate.

Animals↗
PubMed1978

Experimental allergic encephalomyelitis--migration of early T cells from the circulation into the central nervous system.

Study of lymphocytes from the blood of guinea pigs with acute EAE induced by isologous spinal cord in adjuvant reconfirmed that in comparison to normals, the percentage of early (active or high affinity rosetting) T cells decreases dramatically and that these changes can be correlated with clinical signs. In addition, we have investigated matching samples of CNS infiltrating cells recovered by ultrasonication and have found that coinciding with the decrease in early T cells in the circulation, significantly higher levels (P less than 0.001) of these cells appear within the CNS compartment; It is concluded that the decrease of early T cells in the circulation is caused by their migration to the target organ, the CNS.

Animals↗