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Attempts to transfer experimental allergic neuritis with lymphocytes.

Attempts have been made to transfer experimental allergic neuritis (EAN) both by the intraneural and the intravenous injection of cells derived from Lewis rats with the disease into naive recipients of the same strain. Lymph node cells obtained 12 and 15 days after inoculation with bovine dorsal root in Freund's complete adjuvant were injected intraneurally. A small number of demyelinated axons were observed, but clinical weakness was not evident. Lymph node cells, lymph node cells cultured with concanavalin A, or cultured spleen cells from animals with EAN were transferred intravenously to normal rats. Uncultured lymph node cells were transferred to X-irradiated animals. There were no clinical or histological differences between these recipients and controls receiving cells from rats inoculated with Freund's adjuvant alone. The findings are discussed in relation to previous reports of attempts to transmit EAN by cell transfer.

Animals↗
PubMed1987

Cell-mediated immunity to bovine P2 protein and neuritogenic synthetic peptide in experimental allergic neuritis.

Cellular reactivity to bovine P2 protein (P2) and its two synthetic peptides, SP66-78 and SP70-78, was serially examined by the lymphocyte proliferation test in animals with experimental allergic neuritis (EAN). SP66-78 and SP70-78 correspond to residues 66-78 and 70-78 of bovine P2. Proliferative response to SP66-78 as well as P2 appeared at day 7 before the onset of EAN and was clearly manifested at day 14 in the active stage, thereafter disappearing in the stable stage, whereas no response to SP70-78 was detected during the course of the disease. These results suggest that cell-mediated immune response to P2 and the specific part residues 66-78 of P2 play an important role in the pathogenesis of EAN.

Animals↗
PubMed1987

Reduced susceptibility of T cell-deficient rats to induction of experimental allergic neuritis.

Lewis rats were made deficient in T cells by adult thymectomy and lethal irradiation, and then reconstituted with T cell-free bone marrow. Their ability to develop experimental allergic neuritis (EAN) was compared with normal rats. The majority of T cell-deficient rats remained clinically and histologically unaffected, whereas all but one of the normal rats developed severe EAN. Those T cell-deficient animals which succumbed to EAN were found to have a significantly higher percentage of residual blood T lymphocytes than those which did not. Full susceptibility to EAN was restored by an inoculum of whole thoracic duct lymphocytes (TDL) from normal animals but not by TDL depleted of T cells. The results therefore provide direct confirmation that T cells are a requirement for the development of EAN.

Animals↗
PubMed1987

T cell subsets and Ia-positive cells in the sciatic nerve during the course of experimental allergic neuritis.

The changes of T cell subsets and Ia-positive cells in the sciatic nerve during the course of experimental allergic neuritis (EAN) in Lewis rats were studied using immunohistochemical techniques. OX-6+ Ia-positive cells and W3/13+ total T cells were found at the clinical onset of EAN. OX-6+ cells were more numerous than W3/13+ cells during all phases of the disease. In the acute phase, more W3/25+ helper T cells were found than OX-8+ suppressor/cytotoxic T cells in the sciatic nerve. In the recovery phase, W3/25+ cells were slightly fewer than OX-8+ cells. It is suggested that these changes in T cell subsets and Ia-positive cells are related to the self-limiting monophasic course of EAN.

Animals↗
PubMed1988

Responsiveness to P2 of blood- and cauda equina-derived lymphocytes in experimental allergic neuritis in the Lewis rat: preliminary characterisation of a P2-specific cauda equina-derived T cell line.

Experimental allergic neuritis (EAN) was induced in Lewis rats by immunisation with bovine spinal root myelin. Neurological signs appeared on day 12 and persisted for 10-15 days. A transient protein P2-specific proliferative response of circulating mononuclear cells was detected on days 10 and 14 after immunisation but not on days 17 and 35. Mononuclear cells recovered from cauda equina infiltrates on days 14 and 17 showed greater responsiveness to P2 than circulating cells. A P2-specific, interleukin-2-dependent T cell line has been developed from cauda equina (CE)-derived lymphocytes. In adoptive transfer experiments this cell line did not induce EAN but did protect normal recipients from actively induced EAN.

Animals↗
PubMed1988

A T cell epitope for experimental allergic neuritis.

A synthetic peptide representing residues 57-81 of the bovine P2 protein produced severe paralytic experimental allergic neuritis (EAN) in Lewis rats. Peptide 57-81 could also be used to stimulate a P2 protein-specific T cell line to transfer paralytic EAN to naive recipient rats. A smaller peptide representing residues 60-81 produced a milder form of clinical disease. Residues 60-81 are the shortest peptide sequence thus far described which can produce clinical EAN. The structural predictions for the sequence represented by these peptides support the contention that T cell antigenic sites tend to be amphipathic alpha-helical structures.

Animals↗
PubMed1988

Lack of effect of fish oil-enriched diet on experimental allergic neuritis in Lewis rats.

Lewis rats were maintained on a diet enriched with menhaden oil, a rich source of the arachidonic acid (AA) substitute eicosapentaenoic acid (EPA). After dietary manipulation the blood neutrophils showed normal leukotriene (LT)B4 but increased LTB5 concentrations, and the CD4+/CD8+T lymphocyte subset ratio was temporarily perturbed. The dietary manipulation did not affect the severity of actively induced experimental allergic neuritis (EAN).

Animals↗
PubMed1988

Demyelination of sciatic nerve in acute experimental allergic neuritis of the rat. A gel electrophoresis investigation.

Acute experimental allergic neuritis (EAN) of Lewis rats was monitored by clinical and electrophysiological tests for 60 days. Sciatic nerve myelin proteins were analyzed by quantitative microgel electrophoresis and electroimmunoblotting at different clinical stages of the disease. The clinical severity of EAN and the demyelination as measured by electrophysiological tests and myelin protein concentrations in sciatic nerve did not correspond during the course of the disease. Demyelination reached its peak after partial clinical recovery and was still present on day 60. The major peripheral nervous system (PNS) myelin proteins P0, P1 and P2 decreased at different rates during the course of the disease, indicating possible differences in their proteolytic degradation. Treatment with Freund's complete adjuvant (CFA) alone resulted in alterations of membrane and myelin protein patterns challenging the widely held belief that pure CFA is inert with regard to demyelination.

Animals↗
PubMed1989

In vivo monoclonal antibody treatment with Ox19 (anti-rat CD5) causes disease relapse and terminates P2-induced immunospecific tolerance in experimental allergic neuritis.

The role of CD5+ lymphocytes in the recovery phase and on immunospecific protection against experimental allergic neuritis (EAN) was examined in Lewis rats by in vivo treatment with Ox19, a mouse anti-rat CD5 monoclonal antibody. Animals pretreated with the peripheral nerve basic protein P2 and thereby rendered resistant to the disease showed clinical signs of EAN after intraperitoneal (i.p.) Ox19 injection given at the same time as the rechallenge with neuritogenic doses of myelin in Freund's complete adjuvant. Non-pretreated rats recovered from signs of EAN developed a clinical relapse after i.p. Ox19 injections. Taken together, these data suggest an important regulatory role of the CD5 receptor in the immune response.

Animals↗
PubMed1989

Treatment of experimental allergic neuritis with nedocromil sodium.

Peripheral nervous system mast cells degranulate early in the development of experimental allergic neuritis (EAN). This degranulation is associated with the release of vasoactive amines, chemoattractants and myelinolytic proteases which could provide a focus for inflammatory demyelination. To further assess the importance of mast cell degranulation in the development of EAN, we have treated Lewis rats inoculated with peripheral nervous system myelin and complete Freund's adjuvant, with nedocromil sodium, an anti-inflammatory drug with mast cell stabilizing properties. Treatment with nedocromil sodium (100-150 mg/kg), 3 times daily, starting on day 7 post-inoculation, significantly decreases the incidence and the severity of the disease. Histological examination of sciatic nerves confirms the absence of subclinical disease in successfully treated animals. The possible mode of action of the drug is discussed.

Animals↗
PubMed1989

A T cell epitope for experimental allergic neuritis is an amphipathic alpha-helical structure.

The bovine P2 protein is known to produce experimental allergic neuritis (EAN) in Lewis rats. The longest region of amphipathic alpha-helix within the bovine P2 protein was identified as residues 61-72. A synthetic peptide representing this sequence was synthesized and shown to have the ability to (1) produce EAN in Lewis rats by direct sensitization, (2) produce a lymphoproliferative response in a P2-specific T cell line, and (3) stimulate a P2 protein-specific T cell line sufficiently to transfer EAN to naive recipient Lewis rats. Residues 61-72 is the shortest sequence thus far identified that will produce EAN in the Lewis rat and supports the contention that T cell determinants tend to be amphipathic alpha-helices.

Amino Acid Sequence↗
PubMed1990

Suppression of actively induced and passively transferred experimental allergic neuritis by cyclosporin A.

The effect of cyclosporin A (CyA) on experimental allergic neuritis (EAN) was examined. CyA suppressed the development of actively induced EAN. The earlier treatment with CyA was begun, the more effective was its effect. CyA was effective even after the development of clinical signs. In actively induced EAN, cessation of CyA treatment lead to the development of EAN. However, in passively induced EAN, it did not. We could not find any differences in the distribution of infiltrating T cell subsets between the control group and the CyA-treated group.

Animals↗
PubMed1990

The effects of prophylactic cyclosporin A on experimental allergic neuritis (EAN) in the Lewis rat. Induction of relapsing EAN using low dose cyclosporin A.

Experimental allergic neuritis (EAN) was induced in Lewis rats by inoculation with bovine intradural root myelin plus adjuvants. Animals treated with high dose (30 mg/kg) cyclosporin A (CsA) 3 times per week did not develop clinical EAN during the period of CsA treatment, but had an episode of EAN after cessation of CsA treatment. Animals treated with low dose (4 mg/kg) CsA 3 times per week developed EAN during the period of treatment, and after cessation of CsA treatment all of these animals developed relapsing EAN with disease continuing for up to four episodes. In contrast, 30-40% of untreated animals had a mild second episode of EAN but no further attacks. Histological studies performed in treated and untreated animals at the time of clinical episodes revealed inflammation and demyelination in the spinal roots and dorsal root ganglia. When animals were challenged with a second inoculation at age 7 months, one of 15 untreated control animals but none of the CsA treated animals developed an episode of EAN.

Animals↗
PubMed1990

Prednisolone therapy of experimental allergic neuritis in Lewis rats does not induce relapsing or chronic disease.

The effects of therapeutic prednisolone treatment on experimental allergic neuritis (EAN) in Lewis rats were evaluated in a controlled clinical and electrophysiological study. Since steroid therapy has been suspected to cause relapsing or chronic disease, monitoring was extended over 200 days. Short-term steroid treatment (5 days of 15 mg/kg prednisolone, n = 8) with sudden steroid withdrawal was compared with long-term application (30 days, beginning at 7.5 mg/kg) in descending dosage (n = 8). The experiment included saline-injected controls (n = 8) and controls for stress possibly exerted by the handling of the animals. Treatment was begun at the onset of clinical signs. The clinical and electrophysiological data indicated that deterioration, recovery and mild (insignificant) relapse (after day 30 and day 108) occurred in all groups at the same time. Both steroid application schemes significantly (p less than 0.03) attenuated the severity and shortened the duration of EAN. Relapse was not aggravated after steroid treatment. The clinical course and electrophysiological findings were unaltered by the experimental procedures and by mild experimental stress.

Animals↗
PubMed1990

New minimum length requirement for a T cell epitope for experimental allergic neuritis.

The bovine P2 protein induces experimental allergic neuritis (EAN) in Lewis rats. Using synthetic peptides representing regions of the P2 protein sequence and P2-specific neuritogenic T cell lines, we have demonstrated that the minimum peptide length requirement for the T cell epitope for EAN is residues 61-70 of the P2 protein having the sequence EISFKLGQEF. Adding a threonine at the NH2 terminus of this peptide reproduces residues 60-70 of the P2 protein sequence and significantly enhances the neuritogenic capability of this peptide.

Animals↗
PubMed1990

Induction of severe experimental autoimmune neuritis with a synthetic peptide corresponding to the 53-78 amino acid sequence of the myelin P2 protein.

We generated a synthetic peptide (SP-26), corresponding to the amino acid residues 53-78 of bovine P2 protein, which induced severe clinical and pathological characteristics of experimental autoimmune neuritis (EAN) in Lewis rats. Lymph node cell populations from SP-26-immunized rats elicited a proliferative response to the peptide and to the P2 protein. After 16 cycles of antigen stimulation with the peptide, the SP-26 T cell line shows a decreased response to P2, but not to SP-26. Fluorescence-activated cell sorter (FACS) analysis of a SP-26 T cell line indicated the majority of cells to be of CD4+ CD8-. This report demonstrates that the synthetic peptide SP-26 can induce severe EAN in Lewis rats in a dose-dependent manner. Furthermore, specific T cell lines reactive to SP-26 can be generated from the lymph nodes of SP-26-immunized rats.

Animals↗
PubMed1990

Spontaneous chemiluminescence activity of peripheral blood cells during experimental allergic neuritis (EAN).

In 30 Lewis rats the time course of spontaneous monocyte and granulocyte chemiluminescence activity (CLA) during myelin-induced experimental allergic neuritis (EAN) was studied. CLA of blood and peritoneal cells, and clinical, histopathological and electrophysiological findings were compared with data from 14 animals immunized with complete Freund's adjuvant and ten normal Lewis rats. About 12 days post-immunization there was a significant (p less than 0.003) rise in monocyte, but not in granulocyte CLA in EAN animals. CLA correlated significantly (p less than 0.02) with infiltrate formation in nerve roots, preceding clinical or electrophysiological signs of disease by 1-2 days. There was no increase in peritoneal monocyte CLA, which was consistently higher than blood monocyte CLA (p less than 0.002).

Animals↗
PubMed1990

Tumor necrosis factor alpha gene polymorphism in multiple sclerosis and optic neuritis.

The NcoI tumor necrosis factor (TNF alpha) polymorphism was studied in relapsing/remitting multiple sclerosis and monosymptomatic optic neuritis. The frequency of the NcoI marker phenotypes did not differ between healthy controls and the two disease groups. No extra or missing DNA fragments were observed in the disease groups when compared with controls.

Adolescent↗