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PubMed1983

The passive transfer of severe allergic neuritis in Lewis rats with lymphoid cells preincubated with P2 protein.

The passive transfer of both clinical signs and histologic lesions characteristic of allergic neuritis was successfully performed in Lewis rats using pooled spleen and lymph node cells, or T lymphocytes therefrom, if first preincubated in petri dishes with P2 protein for 72 hr. For passive transfer, cells were taken from donors 8-16 days after sensitization with P2 protein or myelin in Freund's complete adjuvant, and administered via the tail vein; clinical signs appeared 12-13 days later. This study supports the importance of cell-mediated immunity in EAN and the antigenic role of the P2 protein.

Animals↗
PubMed1985

Transfer of experimental allergic neuritis with P2-reactive T-cell lines.

Experimental allergic neuritis (EAN) was induced in normal Lewis rats by systemic passive transfer of T-cell lines responding to P2 protein. These cells had predominantly helper phenotype and could induce EAN within 7 days following adoptive transfer. There was no anti-P2 antibody response in the recipients of the P2-reactive cells recovered from donors with high anti-P2 antibody levels. This study provides direct evidence that T cells are important for the induction of EAN. Furthermore, there was no evidence of a pathogenic role for anti-P2 antibody in passive EAN.

Animals↗
PubMed1991

Peptide 53-78 of myelin P2 protein is a T cell epitope for the induction of experimental autoimmune neuritis.

We have recently described the clinical and pathological features of experimental autoimmune neuritis (EAN) in Lewis rats inoculated with varying doses of a synthetic peptide corresponding to the amino acid residues 53-78 of bovine P2 protein (SP-26). Immunization with this synthetic peptide was able to induce severe clinical and pathological characteristics of EAN. We are now reporting that, SP-26 T cell lines derived from spleen and lymph node cell populations of such immunized rats, upon being triggered by SP-26, can adoptively transfer severe clinical and histological signs of EAN to naive syngeneic recipients. The disease appears 7-8 days postinoculation of the cells and persist 5-10 days. The pathological features were indistinguishable from SP-26-induced active EAN which appears 12-15 days after sensitization. Examination of the surface phenotype of the cells that were used for the passive transfer of EAN by FACS analysis, showed majority of the cells to be CD4+, Ia+ cells.

Animals↗
PubMed1983

Cholinesterase activities in the somatic nervous system of rabbits with experimental allergic neuritis.

The allergic inflammatory disorders of the nervous tissue are associated with a complex series of cellular and humoral immune activities and they usually result at least in demyelination, but according to morphologic evidence also in secondary neuronal changes. Using the colorimetric method of Ellman et al. (G. L. Ellman, K. D. Courtney, V. Anders, and R. M. Featherstone, 1961, Biochem. Pharmacol. 7:88-95) the activities of enzymes splitting acetylthiocholine iodide (AThCh) were determined from various parts of the somatic nervous system of rabbits with experimental allergic neuritis (EAN), a primary demyelinating disease of the peripheral nerves. It was found that the total activity of AThCh-splitting enzymes was decreased already in an early phase of the disease in the dorsal root ganglia (DRG). In a well developed phase of the disease the activity of acetylcholinesterase (AChE) seemed to be decreased by 33% in the ventral roots and by a lesser amount in the DRG and the most proximal part of the sciatic nerves. The mechanism of the recorded changes may be related either to specific or to nonspecific immune events or to both. Proteolytic activity released by macrophages in the target tissue may, by inactivating the hydrolytic activity of AChE, at least partly explain these findings. Because the activity of AChE in the structures studied derives from a neuronal origin, our results provide biochemical evidence for the involvement of neurons in the sensory ganglia and of axolemma in the ventral roots in EAN.

Acetylthiocholine↗
PubMed1984

Role of intramuscular enzymatic changes in the development of muscular weakness in rats with experimental allergic neuritis.

We investigated the role of intramuscular enzymatic changes in the development of muscular weakness in rats suffering from experimental allergic neuritis. At an initial stage without apparent clinical symptoms, enzymatic changes of similar types occurred in the muscles of the forelimbs and hind limbs. At a later stage when the weakness appeared in the hind limb but not in the forelimb, dissociation of the pattern of the enzymatic changes occurred between the two limbs. Comparison of the intramuscular enzymatic changes between the two stages and between the two limbs suggested that the increased activities of aminopeptidases and endopeptidases play some important roles in the development of muscular weakness in this experimental model. Low molecular weight protease inhibitors may thus be worthy of a trial in this disease condition.

Aging↗
PubMed1985

Effects of glucocorticoids on experimental allergic neuritis.

Corticosteroids were administered to rats and guinea pigs with experimental allergic neuritis, from the time of inoculation with antigen or from the onset of signs of disease. No statistically significant effects were observed in guinea pigs. In rats, to which large doses of corticosteroids were administered, disease severity was slightly but significantly reduced in both groups and recovery was more rapid in the animals treated from the time of induction of disease. These results were comparable with those obtained in trials of corticosteroids in acute inflammatory polyneuropathy in man, which have also not demonstrated any striking effects.

Animals↗
PubMed1989

High-dose methylprednisolone suppresses experimental allergic neuritis in the Lewis rat.

High dose methylprednisolone (50 mg kg-1, daily) was administered to Lewis rats with experimental allergic neuritis from onset of the disease. Disease severity was reduced and recovery was significantly more rapid than that in saline-injected controls. Histological examination showed reduction of endoneurial edema, cellular infiltration, and demyelination. The results provide experimental evidence supporting the trial of high dose steroids in human demyelinating polyradiculoneuropathy.

Animals↗
PubMed1987

Neuritis of the cauda equina in the horse.

Ultrastructural lesions of the cranial nerves and their ganglia and the autonomic nervous system from 5 cases of neuritis of the cauda equina in the horse are described. They include lysosomal inclusions within the semilunar, geniculate and sympathetic chain ganglia, granulomatous involvement of the coeliaco-mesenteric ganglion and accumulation of axonal organelles in unmyelinated fibres of the great splanchnic nerve, sympathetic chain and oesophageal vagus.

Animals↗
PubMed1975

Recurrent experimental allergic neuritis. An electron microscope study.

Experimental allergic neuritis has been induced in 52 guinea pigs by the inoculation of rabbit peripheral nerve in Freund's adjuvant. The majority of the animals developed an acute monophasic illness after a mean interval of 16 days and, if they survived, recovered fully after an average period of 52 days. Two animals displayed a more chronic course and 1 animal relapsed spontaneously after clinical recovery had occurred. Twenty-three animals that recovered were re-inoculated when recovery was complete and in 4 a relapse was induced. In the remainder, no clinical response was observed, even after repeated reinoculations. The ultrastructural appearances in the animals with a monophasic illness were similar to those previously reported. The appearances differed markedly in those animals that were induced to relapse and were similar to those in the animal that relapsed spontaneously. The findings indicated persistent demyelination and remyelination with striking hypertrophic changes (onion bulb neuropathy). The possible reasons for the differences between the two groups are discussed.

Animals↗
PubMed1976

Relation between Genetic markers and oligoclonal IgG in CSF in optic neuritis.

Thirty patients with acute, unilateral optic neuritis (ON), where re-examination after a mean observation period of 5 years did not reveal any aetiology, were investigated with regard to laboratory abnormalities frequently observed in multiple sclerosis. Eleven patients had oligoclonal IgG in CSF. In 5 of these a measles virus antibody response within the CNS was demonstrable. The remaining 19 patients did not display oligoclonal CSF IgG, nor an antibody response. The major histocompatibility antigens HL-A3 and HL-A7 occurred at similar frequencies in ON and in controls, irrespective of the presence of oligoclonal CSF IgG. The HL-A7 associated MLC determinant LD-7a occurred in ON at a frequency between that observed in controls and in MS. However, an association of the same magnitude as observed in MS was found between ON with oligoclonal CSF IgG and the presence of LD-7a. This association was absent in those ON patients who lacked oligoclonal CSF IgG. The present data indicate that the finding of oligoclonal CSF IgG may increase the risk of developing MS.

Adolescent↗
PubMed1977

Early changes in the Schwann cells in experimental allergic neuritis.

Experimental allergic neuritis (EAN) was induced in guinea-pigs by intradermal injection of rabbit peripheral nerve emulsified in Freund's adjuvant. Both sciatic nerves were obtained between 12--24 hr after clinical symptoms were evident. Several fascicles from each nerve were isolated for histochemical studies with NADH-diaphorase (NADH) and acid phosphatase (AP) applied to teased nerve fibres. Small pieces were processed for electron microscopy, and a fascicle was teased after staining with osmium tetroxide. In isolated nerve fibres stained with histochemical techniques myelin lesions of segmental character were found closely related to inflammatory cells; Schwann cell cytoplasm in contact with mononuclear cells showing a heavy enzymatic activity (NADH and AP). Under polarized light, the underliying myelin showed focal loss of birefringence. Some electron-microscopic pictures suggested active myelin breakdown by mononuclear cells. The possibility of primary Schwann cell damage by mononuclear cells with subsequent demyelination is discussed.

Acid Phosphatase↗
PubMed1980

Alterations of lipid and protein composition in myelin of acute experimental allergic neuritis.

Lipid and protein components of the myelin isolated from the spinal roots of rabbits at the acute stage of experimental allergic neuritis (EAN) and of control rabbits were analyzed. The results obtained from the EAN myelin in comparison with the control myelin were as follows: (1) The content of cholesterol increased and that of cerebroside significantly decreased, while the content of plasmalogen and phospholipid was not changed. The level of cholesterol ester was negligible both in EAN and control myelin. (2) The sum of saturated fatty acids increased while the sum of unsaturated fatty acids decreased. (3) The decrease of the basic proteins P1 and P2 was more noticeable than that of the PO + Y protein. Concomitant to these observations, with 1,6-diphenyl 1,3,5-hexatriene as a fluorescent probe, the microviscosity of the isolated myelin was measured. The results indicated that myelin obtained from EAN was less fluid. Diminished myelin fluidity in EAN was consistent with the results of the lipid and fatty acid analyses.

Acute Disease↗
PubMed1982

The role of macrophages in demyelination in experimental allergic neuritis.

The role of macrophages and serum factors in demyelination in experimental allergic neuritis (EAN) was examined by a simple in vitro method. Cultivated rabbit peritoneal macrophages, preincubated with serum obtained from rabbit EAN produced by sensitization with bovine spinal nerve roots, could agglutinate and phagocytize purified bovine or rabbit peripheral nerve myelin. Sera from normal animals or from controls given adjuvant alone could not. Adhesion and phagocytosis were inhibited if EAN sera were absorbed with peripheral nerve myelin. Rabbit red blood cells were not phagocytized by macrophages exposed to EAN serum. Concomitant to these observations, three lysosomal acid hydrolases: acid proteinase, acid phosphatase and beta-glucuronidase, were assayed with respect to their topographical and chronological distribution. In the group examined at clinical onset, increases in the specific activities were 1.5-3.0-fold in the spinal roots and 1.0-1.5-fold in the sciatic nerves compared with control. The degree of increase in total activities per whole root or sciatic nerve was much higher for specific activities. The topographical distribution of the increase closely corresponded to the histological distribution of EAN lesions. These observations suggested that the increased lysosomal activity originated from lysosomal-rich infiltrating cells. These observations strongly indicated the significant role of macrophages activated by EAN serum in the demyelination of EAN.

Acid Phosphatase↗
PubMed1982

F-wave in experimental allergic neuritis.

The conduction velocity of volleys in motor fibres causing F waves, in addition to distal latency and to maximal motor conduction velocity of volleys in fibres causing the M response, were measured in the hindlimbs of control guinea pigs and rabbits and in those with experimental allergic neuritis (EAN). The spinal roots and sciatic nerves were examined histologically in the animals with EAN. The conduction time to the F wave was abnormal in the presence of normal maximal conduction velocity in fibres causing the M waves in 14% of the guinea pigs and 7% of the rabbits. However, conduction time to the F wave was prolonged in the presence of normal maximal motor conduction velocity in one case where no pathological abnormalities were found in the ventral roots and in some instances, F wave conduction time was within the normal range when ventral root and peripheral nerve demyelination was present. These findings highlight some of the problems in interpretation of F wave studies in man.

Animals↗
PubMed1983

The treatment of experimental allergic neuritis by plasma exchange.

Experimental allergic neuritis (EAN) is a demyelinating disease of the peripheral nervous system that can be induced in laboratory animals. This disorder has been considered to show many similarities to acute inflammatory polyneuropathy (Guillain-Barré syndrome, GBS). Reports that plasma exchange may benefit patients with GBS prompted the investigation of the effect of plasma exchange in EAN. A controlled study was performed on New Zealand White rabbits. Sixteen animals were allocated to control or treatment groups at the onset of the disease. Clinical assessment on days 7 and 14 showed that treated animals were less severely affected neurologically (P = 0.05, day 7; P less than 0.001 day 14), with a commensurate reduction in the severity of the histological lesions in peripheral nerves.

Animals↗
PubMed1983

P2 protein-induced experimental allergic neuritis. An ultrastructural study.

Experimental allergic neuritis (EAN) was induced in 2 groups of inbred Lewis rats by sensitization with P2 protein and peripheral nervous system (PNS) myelin, both purified from bovine intradural roots. Light- and electronmicroscopic study of P2-induced EAN revealed demyelinative lesions in spinal ganglia and root nerves and less frequently in peripheral nerves and root entry zones. Both small and large myelinated fibers were demyelinated, contradictory to the reported selective binding of anti-P2 antibodies to myelin of large fibers. The early lesions were characterised by perivenular lymphocytic infiltration, and subsequent "dissolution" of myelin sheath was associated with invasive of phagocytic cells. The distribution of demyelinative lesions and patterns of demyelination resembled those of PNS myelin-induced EAN except that the disease was milder and dissolution of myelin and intramyelinic edema were more frequently found in P2-induced EAN. The abundance of demyelination in P2-induced EAN strikes contrast to the scarcity of myelin change in experimental allergic encephalomyelitis (EAE) induced by myelin basic protein immunization.

Animals↗
PubMedDate not supplied

Dynamics of Ia-expressing cells and T lymphocytes of different subsets during experimental allergic neuritis in Lewis rats.

Inflammatory cells were characterized by immunohistochemistry, utilizing monoclonal antibodies against cell surface antigens in frozen sections of sciatic nerves and nerve roots of Lewis rats, sacrificed during the course of experimental allergic neuritis. Large numbers of Ia-expressing irregular macrophage-like/dendritic cells, as well as W 3/13 reactive T lymphocytes of both W 3/25 reactive helper and ox8 reactive suppressor/cytotoxic phenotypes were seen within afflicted peripheral nervous tissue at the start of clinical symptoms and at the height of the disease. T lymphocytes of both helper and suppressor/cytotoxic phenotypes decreased concomitant with clinical recovery. During this period demyelination was still extensive and Ia-expressing macrophage-like/dendritic cells were abundant.

Animals↗
PubMed1984

Detection of immune complexes in experimental allergic neuritis.

Circulating immune complexes were assayed in the sera of animals with experimental allergic neuritis (EAN), and immunofluorescent staining and immunohistological examination were performed to clarify the role of immune complexes in the pathogenesis of EAN. The level of immune complexes in the sera of animals with clinical signs of EAN was from 1:32 to 1:64. Control animals showed a titer of immune complexes from 1:2 to 1:4. Animals with EAN showed deposition of immune complexes, which were detected by FITC-conjugated anti-rat IgG or C3-complement, in the vessels of the peripheral nerve. These findings suggest that immune complexes may contribute to the immunopathogenesis of EAN.

Animals↗