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PubMed1997

Fc portion of intravenous immunoglobulin suppresses the induction of experimental allergic neuritis.

To clarify how intravenous immunoglobulin (IVIg) acts on Guillain-Barré syndrome, we investigated the effects of intact-type IVIg treatment on experimental allergic neuritis (EAN) induced by immunizing with synthetic peptide from bovine P2 protein. Treatment with intact-type IVIg (400 mg/kg/day) on days 0, 7, 14, 15 and 16 after immunization prevented the paralysis, whereas treatment with F(ab')2 failed to alter the clinical course. Intact-type IVIg treatment given on days 0 and 1 showed almost the same efficacy. These results suggest that intact-type IVIg is superior to F(ab')2 in ameliorating the clinical course of EAN and that the Fc portion might affect the immune system.

Animals↗
PubMed1997

T-cell receptor V beta-element expression in peripheral nerves of Lewis rats suffering from experimental autoimmune neuritis.

In experimental autoimmune neuritis (EAN), peripheral nerves are infiltrated by T-lymphocytes and macrophages. By RT-PCR and sequence analysis we characterized TCR V beta-element usage in sciatic nerve tissue of Lewis rats suffering from EAN induced by immunization with peripheral myelin antigens. Several TCR V beta-chain sequences were detected, which did not show homology to sequences of P2-reactive T cells published so far. In EAN induced with peripheral nerve myelin, but not with P2-protein or P2 peptide aa 53-78, TCR V beta 8.2 sequences identical to sequences of encephalitogenic myelin basic protein (MBP) reactive T-cells were identified. These results provide further evidence for a contribution of MBP-directed T-cell reactivity to the pathogenesis of myelin induced EAN and may have implications for the pathogenesis of human demyelinating neuropathies.

Animals↗
PubMed1997

Modulation of experimental autoimmune neuritis in Lewis rats by oral application of myelin antigens.

Experimental autoimmune neuritis (EAN) in Lewis rats is a T cell-mediated disease and serves as an animal model of human inflammatory demyelinating neuropathies. EAN can be induced by immunization with complete bovine peripheral nerve myelin (BPM), the myelin protein P2 or its neuritogenic peptide, each emulsified in complete Freund's adjuvant (CFA). The present study evaluates the effect of oral tolerization with BPM or P2 protein on the development of actively induced EAN. Oral administration of BPM strongly suppressed clinical and histological signs of EAN subsequently induced by BPM/CFA, but feeding of P2 protein alone did not affect its course. In contrast, feeding of BPM did not mitigate the course of EAN subsequently induced by immunization with neuritogenic P2 peptide/CFA. Oral therapy with BPM after onset of myelin-induced EAN only slightly ameliorated the further course of disease, but significantly reduced lethality of this severe form of disease. The findings suggest that immunogenicity of the antigens fed determine strength of tolerance, that downregulation of EAN occurs at the site of immunization and not in the nerve, and that active suppression rather than specific anergization is operative in mediating resistance to EAN. However, only partial tolerance to myelin-induced EAN was achieved in naive animals by transfer of spleen/LN cells from rats orally tolerized with BPM. Although methodic factors may have limited the effect of the cells, the result is suggestive of some contribution of anergy to oral tolerance in the present model. Cholera toxin and LPS were identified as oral adjuvants for BPM and prolonged the state of tolerance. However, LPS exhibited proinflammatory properties if EAN was induced early after BPM/LPS-feeding. Thus, oral application of a mixture of myelin components in combination with cholera toxin may be a useful treatment for chronic inflammatory neuropathies considered autoimmune in nature.

Adjuvants, Immunologic↗
PubMed1998

Cytokine production and the pathogenesis of experimental autoimmune neuritis and Guillain-Barré syndrome.

Acute inflammatory demyelinating polyradiculoneuropathy (Guillain-Barré syndrome, GBS) and its animal model experimental autoimmune neuritis (EAN) are prototypes of T cell-mediated autoimmune diseases affecting the peripheral nervous system (PNS). Perivascular accumulation of macrophages and T lymphocytes in the PNS, and high levels systemically of PNS myelin antigen-reactive T cells are characteristic features of both diseases, thereby suggesting a pathogenic role for immunoregulatory cytokines. Here we summarise recent studies that have clearly documented that Th1/Th2/Th3 cytokines are differently upregulated during various clinical phases of EAN and GBS. The observations indicate that the role of cytokines in immune regulation and autoimmune disease is more complex than a simple Th1-Th2 dichotomy would suggest. New treatments may be searched for that counteract this complex cytokine imbalance. Treatments with antibodies that selectively target certain pro-inflammatory cytokines, as well as with immunomodulatory preparations that promote cytokines that beneficially influence the disease course should be in focus of future therapeutic trials.

Animals↗
PubMed1998

The expression of cytokine mRNA in the cauda equina of Lewis rats with experimental allergic neuritis.

Autoreactive CD4+ T cells can transfer experimental allergic neuritis (EAN) to naive recipients. In order to further analyze the role of these T cells and their corresponding cytokines in EAN, we studied the expression of mRNA for IFN-gamma, IL-4, and IL-10 in the cauda equina of rats with EAN using a quantitative competitive reverse transcriptase PCR method. Nerves were studied on days 0 (pre-immunization), 10 (disease onset), 13 (clinical progression), 16 (disease peak), as well as 20, 24, and 34 post immunization (recovery). IFN-gamma messages increased at disease onset and peaked at day 13 p.i. IL-10 message remained at a very low level at disease onset and surged at day 16. Both messages were low in recovery stage. IL-4 message was undetectable at any time point. These data suggest a pro-inflammatory role of IFN-gamma and anti-inflammatory role of IL-10 in EAN lesions. It is also possible that a clonal switch from Th1 to Th2 occurs in EAN lesions during the disease course.

Actins↗
PubMed1998

Treatment with P2 protein peptide 57-81 by nasal route is effective in Lewis rat experimental autoimmune neuritis.

Experimental autoimmune neuritis (EAN) is a CD4+ T cell-mediated autoimmune disorder of the peripheral nervous system (PNS) that can be actively induced in susceptible animal species and strains by active immunization with PNS myelin + Freund's complete adjuvant (FCA). EAN represents an animal model for studying the immunopathogenesis and treatment of Guillain-Barré syndrome (GBS), which is a major inflammatory demyelinating disease of the PNS in humans. Here, we report that treatment by nasal administration of the neuritogenic peptide 57-81 of the PNS myelin component, P2 protein, dose-dependently suppressed EAN severity and shortened clinical EAN. Clinical EAN relapse induced by rechallenge with BPM + FCA was also prevented in EAN rats receiving high dose P2 peptide. P2 peptide induced suppression of EAN was associated with PNS antigen specific T cell hyporesponsiveness reflected by lymphocyte proliferation, numbers of PNS antigen-reactive IFN-gamma secreting and IFN-gamma mRNA expressing lymph node cells, but elevated levels of PNS antigen reactive TGF-beta mRNA secreting cells. Reduced CD4+ T cell and macrophage infiltrations within the PNS were also observed. Based on these observations, nasal autoantigen administration should be further evaluated, considering its possible future use in GBS.

Administration, Intranasal↗
PubMed1998

The disintegrin domain of ADAM 8 enhances protection against rat experimental autoimmune encephalomyelitis, neuritis and uveitis by a polyvalent autoantigen vaccine.

Targeting peptides have potential as components of recombinant vaccines. Here, we have analyzed a set of structurally diverse peptides fused to a polyepitope vaccine in prevention of rat generalized autoimmunity of the nervous system (GANS), a combined model of experimental autoimmune encephalomyelitis (EAE), neuritis (EAN) and uveoretinitis (EAU). The peptide sequences studied included the endothelial-monocyte-activating polypeptide II (EMAP II), the allograft inflammatory factor-1 (AIF-1), and the interferon-gamma-inducing factor (IGIF, IL-18). Further, a variety of adhesive peptides were tested, including the disintegrin domain of mouse ADAM 8. Interestingly, this disintegrin domain considerably increased the effect of the polyepitope vaccine. Of the other peptides, only IL-18 enhanced tolerance induction, but was less effective than the ADAM 8 disintegrin peptide. In conclusion, disintegrin domains will be valuable leads in the development of targeting peptides for immunointervention.

ADAM Proteins↗
PubMed1998

Soluble ICAM-1, demyelination, and inflammation in multiple sclerosis and acute optic neuritis.

We measured sICAM-1 in paired samples of serum and cerebrospinal fluid (CSF) from patients with an attack of multiple sclerosis (MS) (n = 50) and patients with acute monosymptomatic optic neuritis (ON) as a possible first attack of MS were also included (n = 25). Based on calculations of extended indices we found evidence of intrathecal synthesis of sICAM-1 both in patients with clinically definite MS and in patients with idiopathic ON compared to neurological control subjects. The amount of intrathecally synthesized sICAM-1 correlated significantly to the CSF leukocyte count and to the concentration of myelin basic protein in the CSF. The serum concentrations of sICAM-1 were not increased in patients with demyelinating disease compared to the neurological control subjects.

Acute Disease↗
PubMed1999

CP-10, a chemotactic peptide, is expressed in lesions of experimental autoimmune encephalomyelitis, neuritis, uveitis and in C6 gliomas.

CP-10 (chemotactic protein of m.w. 10,000) is a member of the S100 superfamily of Ca2+ binding peptides, which has potent chemotactic activity for murine and human myeloid cells. Here we report on the generation of monoclonal antibodies against CP-10 and accumulation of CP-10+ cells during experimental autoimmune encephalomyelitis (EAE), neuritis (EAN), uveitis (EAU) and in experimentally transplanted C6 gliomas. During acute inflammation, CP-10 is mainly expressed by large ED1+ monocytic perivascular cells that accumulate at days 11-14. CP-10+ cells are predominantly located in areas of cellular infiltration but are as well found in the meninges and infiltrating the brain parenchyma. In transplanted gliomas, CP-10+ cells are located exclusively within the tumor parenchyma. Using double labeling experiments, other cells participating in the inflammatory reaction were found to express CP-10, like few lymphoblastic W3/13+ cells in the vicinity of the inflammatory infiltrate.

Animals↗
PubMed1999

Antigen-specific immunosuppression: nasal tolerance to P0 protein peptides for the prevention and treatment of experimental autoimmune neuritis in Lewis rats.

Experimental autoimmune neuritis (EAN) is an autoimmune inflammatory demyelinating disease of the peripheral nervous system (PNS), and represents an animal model of the human Guillain-Barré syndrome (GBS). In this study, we report that nasal administration of the neuritogenic peptide 180-199 and of the cryptic peptide 56-71 of the rat neuritogenic P0 protein of peripheral nerve myelin prevents EAN and attenuates ongoing EAN. Both peptides effectively decreased the severity and shortened clinical EAN. Both a prophylactic and a therapeutic approach proved to be beneficial. These effects were associated with T and B cells hyporesponsiveness to the peptide antigens, reflected by downregulated Th1 cell responses (interferon-gamma secretion) and macrophage function, whereas Th2 cell responses (IL-4 secretion) and transforming growth factor-beta mRNA expression were upregulated.

Administration, Intranasal↗
PubMed1999

Induction of experimental autoimmune neuritis in CD4-8-C57BL/6J mice.

The C57BL/6J mice strain is known to be reputedly resistant to induction of experimental autoimmune neuritis (EAN), an animal model of Guillain-Barré syndrome in humans. Here we describe the induction of EAN in mice of the C57BL/6J background by transfer into naive syngeneic recipients bovine peripheral nerve myelin (BPM)-primed donor lymph node cells that had been stimulated in vitro with the bovine peripheral nervous system (PNS) myelin P2 protein peptide 57-81 followed by challenge with BPM, Freund's complete adjuvant and pertussis toxin. EAN was more severe, both clinically and histologically, and accompanied by extensive infiltration of inflammatory cells and demyelination in peripheral nerves when examined on day 30 after transfer of primed T cells from CD4- 8- mice into identical naive hosts than after transfer of cells from primed wild type, CD4-/- or CD8-/- mice to corresponding recipient animals. EAN in CD4-8- mice was also associated with elevated numbers of P2 peptide-reactive interferon-y (TFN-gamma) secreting cells and alphabeta T cells were present in lymph nodes and spleens. The data suggest that PNS myelin activated T cells from an EAN-resistant mice strain are capable of homing to the PNS. The expanded CD4-8- alphabeta T cells may have helper and effector functions, related to initiation of EAN in the CD4-8- mice. Lack of CD4+ and CD8+ expressing cells does not prevent the initiation of an autoimmune disease.

Animals↗
PubMed1999

Costimulatory molecules B7-1 and B7-2 on CSF cells in multiple sclerosis and optic neuritis.

The aberrant expression of B7 costimulatory molecules is involved in the pathogenesis of autoimmune diseases and overexpression of B7-1 was found in inflammatory multiple sclerosis (MS) lesions. We here report that costimulatory molecules B7-1 and B7-2 are expressed on cerebrospinal fluid (CSF) monocytes and B-lymphocytes from patients with MS, optic neuritis (ON) and other inflammatory central nervous system (CNS) diseases. In patients with ON but not MS, increased expression of B7-2 was detected as compared to non-inflammatory controls. The expression of B7-1 in MS and ON patients correlates with disease duration but not with relapses in patients with MS indicating a role in early disease but not as a reliable marker of disease activity at later stages of MS.

Antigens, CD↗
PubMed1999

Chemokine mRNA expression in the cauda equina of Lewis rats with experimental allergic neuritis.

Chemokines play an important role in the migration of leukocytes to inflammatory sites. In this study, using the quantitative competitive reverse transcriptase PCR method, we analyzed sequential expression of certain chemokine mRNAs in the cauda equina (CE) of rats with experimental allergic neuritis (EAN). Interferon-gamma-inducible protein (IP)-10, monocyte chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1alpha, the regulated upon activation normal T cell expressed and secreted chemokine (RANTES), and lymphotactin were analyzed on days 0 (pre-immunization), 7 (preclinical stage), 10 (disease onset), 13 (clinical progression), 17 (disease peak), as well as on days 20, 24, and 34 post-immunization (p.i.) (recovery). MCP-1 message increased at the preclinical stage and peaked at day 17 p.i. The increase in the early stage was not detected in other tissues, indicating peripheral nerve-specific upregulation. MIP-1alpha and IP-10 messages surged at day 13, then returned to low in the recovery stage. RANTES message increased at day 13 and peaked at day 17 p.i.; however, unlike other chemokines, it showed a second peak of expression on day 24. Lymphotactin message was undetectable at any time point. MCP-1 protein was detected immunohistologically in endothelial cells at day 7 p.i. The sequential expression of these chemokines in relation to the inflammatory process in the nerve leading to demyelination is discussed.

Animals↗
PubMed1999

Dynamics of production of MIP-1alpha, MCP-1 and MIP-2 and potential role of neutralization of these chemokines in the regulation of immune responses during experimental autoimmune neuritis in Lewis rats.

Experimental autoimmune neuritis (EAN) is an inflammatory autoimmune demyelinating disease of the peripheral nervous system (PNS) and represents an animal model of Guillain-Barré syndrome (GBS), which is a major inflammatory demyelinating disease of the PNS in humans. In the present study, the dynamics of the expression of the chemokines macrophage inflammatory protein-1alpha (MIP-1alpha), MIP-2 and monocyte chemotactic protein-1 (MCP-1) were determined in the sciatic nerves of EAN rats. Additionally, the effect of neutralizing antibodies against MIP-1alpha, MIP-2 and MCP-1 on the clinical course of EAN and the chemokine expression was investigated. The maximum of MIP-1alpha positive cells in the sciatic nerves was seen on day 14 post immunization (p.i.) correlating with the development of severe clinical signs. Administration of an anti-MIP-1alpha antibody suppressed the clinical signs of EAN and inhibited inflammation and demyelination in the sciatic nerve. Peak numbers of MCP-1 positive cells in the sciatic nerves were detected on day 7 p.i. Administration of an anti-MCP-1 antibody caused a delay of onset of EAN. However, 4 of the 6 EAN rats receiving the anti-MCP-antibody showed the same degree of inflammatory cell infiltration and demyelination in the sciatic nerves as sham-treated EAN rats, whereas only 2 EAN rats had less inflammation and demyelination. The numbers of MIP-2 positive cells reached a maximum on day 21 p.i. Anti-MIP-2 antibody failed to suppress the clinical signs of EAN and the inflammation and demyelination in the sciatic nerves. Only administration of the anti-MIP-1alpha antibody resulted in a significant reduction in the number of chemokine (MIP-1alpha)-positive cells and ED1-positive macrophages in the sciatic nerves. The present results demonstrate that MIP-1alpha and MCP-1 may play a role in the immunopathogenesis of EAN, and that MIP-1alpha induced trafficking of inflammatory cells can be inhibited by immunoneutralization. Further elucidation of the regulation and coordination of MIP-1alpha and MCP-1 production may lead to new therapeutic approaches to GBS in humans.

Animals↗
PubMed2000

Characterization of T cell receptor associated with the development of P2 peptide-induced autoimmune neuritis.

To characterize experimental autoimmune neuritis (EAN)-inducing T cells in more detail, we performed CDR3 spectratyping analysis and found oligoclonal expansion of several Vbeta spectratypes in nerve-infiltrating T cells. Vbeta5 expansion was observed all the stages examined, whereas Vbeta8.2 and Vbeta17 expansion was mainly found at the peak and preclinical stages, respectively. Since Vbeta5 expansion persists throughout the course of the disease, Vbeta5+ T cells are judged to be the main effector cells. Vbeta8.2+ and Vbeta17+ T cells may also be pathogenic but are not the main effectors because expansion of these spectratypes was found at a limited period of time. Sequence analysis revealed that Vbeta5, Vbeta8.2 and Vbeta17 spectratype-derived TCR clones possess their own dominant sequences in the CDR3 region with no homology among the clones. These findings suggest that polyclonally activated T cells are involved in the formation of the nerve lesion. Furthermore, vaccination with Vbeta5 DNA, but not with Vbeta10 DNA, suppressed the development of EAN significantly. Collectively, these findings indicate that determination of autoimmune disease-associated TCR by CDR3 spectratyping provides useful information for designing TCR-based immunotherapy for the disease.

Amino Acid Sequence↗
PubMed2005

[Optic neuritis associated with infliximab].

Infliximab is a chimeric human-murine monoclonal antibody of the IgG1 type with a high affinity and specificity for tumor necrosis factor alpha (TNFalpha). Infliximab was used in Crohn disease, rheumatoid arthritis, spondyloarthropathy, juvenile idiopathic arthritis, Behcet's disease, Wegener's granulomatosis, HLA-B27-associated uveitis and chronic severe refractory uveitis. Reported adverse effects of this treatment were infections, development of antinuclear antibodies and anti double-stranded DNA, lymphomas, and exacerbation of demyelinating disease. We report a case of infliximab-associated optic neuritis with favorable outcome after systemic steroid treatment.

Antibodies, Monoclonal↗
PubMed1996

Vestibular neuritis: clinical-pathologic correlation.

Postmortem examination of the brain and temporal bones of a patient with well-documented vestibular neuritis showed selective neuronal loss in Scarpa's ganglia on the side with absent caloric response. There was loss of hair cells and an "epithelialization" of the utricular macule and semicircular canal cristae on the deafferented side, and synaptic density in the vestibular nuclei on the deafferented side was decreased compared with that on the normal side. All findings were consistent with an isolated viral infection of Scarpa's ganglia. This is the first description of the effects of chronic deafferentation on the vestibular sensory epithelia and the vestibular nuclei in a human being.

Aged↗
PubMed1988

Migrant sensory neuritis of Wartenberg. A case history.

A case history of a patient with a Migrant sensory neuritis of Wartenberg is presented. In this syndrome several isolated cutaneous nerves are affected, apparently due to traction lesions. This benign disease should be differentiated from other, more serious neurological diseases.

Adult↗