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PubMed2002

Changes in axonal morphology in experimental autoimmune neuritis as studied by high b-value q-space (1)H and (2)H DQF diffusion magnetic resonance spectroscopy.

Experimental autoimmune neuritis (EAN) has been studied in rat sciatic nerves by a combination of high b-value (1)H and (2)H double quantum filtered (DQF) diffusion MRS. The signal decays of water in the (1)H and (2)H DQF diffusion MRS were found to be not monoexponential and were analyzed using the q-space approach. The q-space analysis of the (1)H diffusion data detected two diffusing components, one having broad and the other having narrow displacement profiles. These components were shown to be very sensitive to the progression of EAN disease. The q-space parameters were found to be abnormal at day 9 postimmunization before the appearance of clinical signs. The assignment of the component with the narrow displacement profile to axonal water has been corroborated by the (2)H DQF diffusion MRS results. The displacement and the relative population of this slow and restricted diffusing component followed the processes of demyelination, axonal loss, and remyelination that occur in EAN. The displacements extracted from the slow-diffusing component with the narrow displacement correlated well with the average size of the axons as deduced from electron microscopy (EM). The component with the broad displacement showed significant changes which were attributed to the formation of endoneurial edema. This observation was also corroborated by the (2)H DQF diffusion MRS experiments. It seems, therefore, that q-space analysis of high b-values diffusion MRS is a promising new approach for early detection and better characterization of the different pathologies associated with EAN. This study demonstrates the utility of high-b-value q-space diffusion MRS for studying white matter-associated disorders in general.

Animals↗
PubMed2002

Assessment of experimental autoimmune neuritis in the rat by electrophysiology of the tail nerve.

The assessment of experimental autoimmune neuritis (EAN) by electrophysiological studies of the sciatic innervation of the plantar muscle may be complicated by local inflammation. We therefore utilized the tail nerve-muscle system to monitor disease progression in 20 rats with EAN and 10 control rats. Early changes were detected in motor nerve conduction velocity (32.06 +/- 1.85 m/s versus 43.57 +/- 3.98 m/s in controls, P < 0.001) at 15 days postimmunization (DPI), and conduction block (70.6 +/- 9.4% compared to 12.4 +/- 3.4%, P < 0.001) at 22 DPI. No consistent conduction block (22.4 +/- 10.4%) was found in the plantar muscle measurements. The tail nerve response of EAN rats demonstrated severe temporal dispersion at 43 DPI, which returned to normal at 135 DPI, although motor nerve conduction velocity values were still lower than in controls (24.4 +/- 0.9 m/s, P < 0.001). The tail nerve may be a useful addition to electrophysiological studies in this model of the Guillain-Barré syndrome.

Animals↗
PubMed2002

New cyclooxygenase-2 inhibitors for treatment of experimental autoimmune neuritis.

We analyzed two new cyclooxygenase-2 (COX-2) inhibitors, celecoxib (SC-58635) and meloxicam, for the treatment of experimental autoimmune neuritis (EAN) in rats. Celecoxib and meloxicam significantly reduced clinical EAN score and histopathological damage of the sciatic nerve. They induced no serious side effects, whereas indomethacin used as a control caused severe intestinal ulceration and dysfunction of liver and kidney. These findings suggest that the new COX-2 inhibitors may be useful as additional therapeutic agents for patients with Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy.

Animals↗
PubMed1990

Early myelin lesions in experimental allergic neuritis.

We examined the evolution of demyelination in spinal roots of Lewis rats immunized with whole nerve and complete Freund's adjuvant. Roots were morphologically normal until 11 days after immunization, when we found endoneurial edema and myelin vesiculation in the absence of mononuclear cell contacts. Macrophage-associated myelin stripping was not detected until day 12. Macrophage infiltrations were extensive by day 14, but lymphocytes were sparse. These observations indicate that in experimental allergic neuritis, myelin injury may occur before macrophage-mediated demyelination, and provide support for an early role of serum factors in the development of this disorder.

Animals↗
PubMed1994

Postsurgical idiopathic brachial neuritis.

Idiopathic brachial neuritis (IBN) is a well-recognized clinical syndrome characterized by brachial pain followed by a patchy amyotrophy of muscles in the shoulder girdle and arm innervated by individual branches of the brachial plexus. Postsurgical IBN has not been widely recognized since Parsonage and Turner's original description in which 10% of patients had antecedent surgery. We present 6 patients who 1-13 days postoperatively developed signs and symptoms which met the clinical and electrophysiologic criteria for IBN. Postsurgical neuralgic amyotrophy is an under-recognized clinical entity which in most cases is ascribed to brachial plexus stretch injuries occurring during anesthesia. Early recognition of this condition may prevent unnecessary surgical exploration and allow for a more accurate prediction of functional recovery.

Adult↗
PubMed1996

Conformation of an antigenic determinant for experimental autoimmune neuritis.

The conformation of SP-26, the synthetic peptide (residues 53-78) of myelin P2 protein that causes experimental autoimmune neuritis (EAN) in the peripheral nervous system, has been investigated in D2O using Fourier transform infra-red spectroscopy. Turns were found in 26% of the residues in the peptide, with rest of the residues in random coil (72%). The presence of 26% turns agrees well with the number of residues forming three turns in the antigenic region of the intact protein and the number of turns correlates well with the severity of EAN. Since turns also exist in peptides inducing experimental autoimmune encephalomyelitis, the central nervous system counterpart of EAN, turn structure may be a common structural motif for these closely related autoimmune neurological disorders.

Amino Acid Sequence↗
PubMed1995

Leber's hereditary optic neuropathy (LHON)-related mitochondrial DNA sequence changes in italian patients presenting with sporadic bilateral optic neuritis.

Eighteen Italian patients presenting with sporadic, bilateral, simultaneous, or sequential optic neuritis (ON) were evaluated for 14 base changes in mitochondrial DNA (mtDNA) previously found associated with Leber's hereditary optic neuropathy (LHON), aiming to identify at a molecular level LHON cases with nontypical phenotypes. During a 36-month follow-up, 11 ON patients developed clinical or laboratory features allowing diagnosis of clinically definite multiple sclerosis (MS). None was positive for any of the "primary" LHON-associated mutations. However, single or multiple "secondary" LHON-associated sequence changes at 4216/ND1, 4917/ND2, and 13708/ND5 were detected in ON and ON-MS patients. MS controls without visual failure as well as healthy control subjects harbored the same base changes at similar frequencies. In addition, coexistence of three sequence changes was found in two cases (1 ON-MS patient and 1 MS control patient). We also report finding two new neutral sequence base changes in the ND-4 gene which were identified by SSCP and confirmed by automated DNA sequence analysis. The results suggests that these secondary mutations do not contribute to MS susceptibility in these patients, but rather represent neutral mitochondrial DNA polymorphisms. In addition, whether there are biochemical abnormalities related to single and multiple secondary mtDNA sequence changes remain to be demonstrated.

Adult↗
PubMed1993

Induction of peripheral tolerance with peptide-specific anergy in experimental autoimmune neuritis.

Neuritogenic T cells specific for SP-26, a synthetic peptide (residue 53-78) of myelin P2 protein that causes experimental autoimmune neuritis (EAN), use the same T cell receptor (TCR) V gene family (V beta 8) that can induce experimental autoimmune encephalomyelitis (EAE) in Lewis rats. Tolerance to autoregulatory T cells may be induced in rats by intravenous (iv) administration of antigen-coupled splenocytes; however, the mechanisms that lead to altered immune reactivity are not well understood. Here we demonstrate that SP-26, when coupled to syngeneic spleen cells and administered iv, either before or after disease induction, markedly inhibited development and expression of clinical signs and histological changes of EAN. The induction of tolerance by this method was peptide-specific and MHC-restricted. We showed previously that T cells involved in EAN utilize the T cell antigen receptor V beta 8, whereas less than 5% of normal rat peripheral T cells express V beta 8. We have examined T lymphocytes from tolerized rats to determine the presence or absence of V beta 8(+)-bearing cells in order to determine the mechanism of tolerance. V beta 8 cells were undetectable by Northern blot analysis in the lymph nodes of unimmunized animals but easily detected in SP-26-primed and tolerized rats. In addition, spleen cells isolated from tolerized animals were anergic and failed to proliferate in response to SP-26, but retained responsiveness to IL-2 and Con A stimulation. Thus, the peptide-specific unresponsiveness that can be induced in rats with EAN, a T-cell-mediated process that is MHC-restricted and utilizes the T cell receptor V beta 8, occurs while V beta 8 transcripts remain readily detectable in spleen and lymph node cells. The detection of V beta 8-bearing T cells requires the development of antibodies specific for this rat surface protein.

Amino Acid Sequence↗
PubMed1994

Regulation of experimental autoimmune neuritis by transforming growth factor-beta 1.

Experimental autoimmune neuritis (EAN) is a T-cell-mediated autoimmune disease characterized by demyelination and mononuclear cell infiltration of the peripheral nervous system. It is induced in Lewis rats by administration of myelin P2 protein or a synthetic peptide (SP-26) corresponding to amino acid residues 53-78 of bovine P2 protein. The effects of transforming growth factor-beta 1 (TGF-beta 1) on the clinical signs, histological changes, cell-mediated immune responses, and secretion of interferon-gamma (IFN-gamma) by lymphoid cells of rats with EAN were examined. Systemic administration of TGF-beta 1 markedly inhibited the clinical signs and histological changes of EAN when given intraperitoneally every other day for Days 0 through 18. In addition, it decreased proliferative responses and reduced the delayed-type hypersensitivity (DTH) response to SP-26 compared to control rats. The reduction in clinical severity correlated with skin test unresponsiveness (DTH) to the disease-inducing agent (SP-26) as well to decreased cellular responsiveness to the antigen in vitro. The decrease in cellular responsiveness extended to a decrease in at least one T cell lymphokine, IFN-gamma. The profound effect of TGF-beta on disease progression in EAN, a T-cell-mediated process, is consistent with a direct effect of this growth factor on T lymphocytes.

Amino Acid Sequence↗
PubMed1997

IL-10 suppresses experimental autoimmune neuritis and down-regulates TH1-type immune responses.

Experimental autoimmune neuritis (EAN) is a CD4+ T cell-mediated monophasic inflammatory disorder of the peripheral nervous system (PNS). Cellular mechanisms, including macrophage and T cell infiltration, and cytokines like IFN-gamma and TNF-alpha are intimately involved in the pathogenesis of EAN. Interleukin 10 (IL-10) is a TH2-type cytokine that suppresses monocyte and TH1 cell functions. We examined the effect of recombinant human IL-10 (rHuIL-10) in EAN. When administered from the start of immunization with bovine peripheral myelin emulsified in Freund's complete adjuvant, IL-10 effectively suppressed and shortened clinical EAN. Even when given after Day 12 post immunization (pi) after clinical EAN had been established, IL-10 also effectively suppressed the severity of EAN. Pheripheral nerve myelin antigen-reactive IFN-gamma-secreting TH1-like cells were decreased in lymph nodes from IL-10-treated compared to control EAN rats. PNS autoantigen-induced T cell proliferation and B cell responses were not affected. P2 protein-reactive IFN-gamma, TNF-alpha, IL-1 beta, and IL-6 mRNA-expressing lymph node cells were also downregulated in IL-10-treated compared to control EAN rats at Day 14 and 26 pi, while P2-reactive IL-4 mRNA-expressing cells were upregulated throughout treatment. Also, in IL-10-treated EAN rats, upregulated anti-P2 IgG1 and downregulated IgG2a were observed. Our results clearly show that rHuIL-10 can suppress clinical EAN, and this suppression is associated with downregulation of TH1 responses and macrophage function and upregulated TH2 responses.

Animals↗
PubMed1997

Cytokine dichotomy in peripheral nervous system influences the outcome of experimental allergic neuritis: dynamics of mRNA expression for IL-1 beta, IL-6, IL-10, IL-12, TNF-alpha, TNF-beta, and cytolysin.

Experimental autoimmune neuritis (EAN) is a T-cell-mediated autoimmune disease of the peripheral nervous system (PNS) that can be actively induced in Lewis rats by immunization with bovine PNS myelin and Freund's complete adjuvant. EAN is used as an animal model of the Guillain-Barré syndrome (GBS) in humans. To study the potential role of cytokines in EAN, we used in situ hybridization to detect mRNA expression of interleukin 1 beta (IL-1 beta), IL-6, IL-10, IL-12, tumor necrosis factor-alpha (TNF-alpha), TNF-beta, and cytolysin in sciatic nerve sections over the course of EAN. Cells expressing IL-1 beta and IL-6 mRNA appeared early and peaked on Day 7 postimmunization (p.i.), i.e., at onset of clinical signs of EAN, consistent with a role of these cytokine in an early immune response leading to autoaggressive immunity in EAN. TNF-alpha, TNF-beta, and IL-12 mRNA expression was maximally upmodulated on Day 14 p.i., i.e., at height of clinical EAN, favoring a role for these cytokines in disease development. On the contrary, transcription of cytolysin and IL-10 in sciatic nerves reached maxima during clinical improvement of EAN. The data argue for a major proinflammatory role for IL-1 beta, IL-6, TNF-alpha, TNF-beta, and IL-12 and a disease downregulating function for both cytolysin and IL-10 at the target site in EAN. These findings have relevance for future studies on pathogenesis and treatment of GBS in humans.

Animals↗
PubMed2000

Enhancement of acute phase and inhibition of chronic phase of experimental autoimmune neuritis in Lewis rats by intranasal administration of recombinant mouse interleukin 17: potential immunoregulatory role.

Experimental autoimmune neuritis (EAN) is a CD4(+) T-cell-mediated demyelinating disease of the peripheral nervous system (PNS). We examined the effect of recombinant mouse interleukin 17 (rmIL-17) on chronic EAN induced in Lewis rats by inoculation of P2 57-81 peptide in Freund's complete adjuvant. Animals were treated nasally for 6 days with either 0.1 or 0.9 microg/rat/day rmIL-17 from the onset of neurological signs, i.e., days 9 to 14 postimmunization (p.i.). Prolonged follow-up demonstrated a chronic course in control and rmIL-17-treated rats. Treated rats had more severe disease initially (days 18-36 p.i.) with a stronger enhancing effect observed with the higher rmIL-17 dose. At day 19 rmIL-17-treated rats showed increased infiltration of inflammatory cells into the sciatic nerve, more severe demyelination, augmented proliferation of regional lymph node cells, and increased serum levels of tumor necrosis factor-alpha. After the initial phase of disease enhancement the IL-17-treated EAN rats improved gradually and ultimately recovered completely, whereas the control EAN rats remained affected until the end of the observation (day 120 p.i.). The lower dose of rmIL-17 induced an earlier recovery from clinical deficits than the higher one. The results indicate that IL-17 plays an immunoregulatory role in chronic EAN which could have implications for immunomodulatory treatments of chronic autoimmune disease of the PNS.

Acute Disease↗
PubMed2001

Suppression of autoimmune neuritis in IFN-gamma receptor-deficient mice.

Experimental autoimmune neuritis (EAN) is an animal model of the human disease Guillain-Barré syndrome. In this autoimmune inflammatory disease, CD4(+) T cells mediate demyelination in the peripheral nervous system (PNS). Infiltrating macrophages and T cells as well as cytokines like interferon (IFN)-gamma are intimately involved in causing pathogenic effects. To investigate the role of IFN-gamma in cell-mediated EAN, IFN-gamma receptor-deficient mutant (IFN-gammaR(-/-)) C57BL/6 mice and corresponding wild-type mice were immunized with P0 peptide 180-199, a purified component of peripheral nerve myelin, and Freund's complete adjuvant. IFN-gammaR(-/-) mice exhibited later onset of clinical disease. The disease was also less severe than in wild-type mice. Fewer IL-12-producing but more IL-4-producing cells were found in sciatic nerve sections from IFN-gammaR(-/-) mice than from wild-type mice on day 24 postimmunization, i.e., at the peak of clinical EAN. At the same time, IFN-gammaR(-/-) mice had less infiltration of inflammatory cells, including macrophages, CD4(+) T cells, and monocytes, into sciatic nerve tissue and less demyelination. However, numbers of IFN-gamma-secreting cells from the spleen were significantly augmented in the IFN-gammaR(-/-) mice, reflecting a failure of negative feedback circuits. The IFN-gammaR deficiency did not affect the production of anti-P0 peptide 180-199-specific antibodies. These results indicate that IFN-gamma contributes to a susceptibility for EAN in C57BL/6 mice by promoting a Th1 cell-mediated immune response and suppressing a Th2 response.

Animals↗
PubMed2002

CD4 and CD8 T cells, but not B cells, are critical to the control of murine experimental autoimmune neuritis.

Experimental autoimmune neuritis (EAN) is a T cell-mediated autoimmune disease of the peripheral nervous system that duplicates the clinical, pathological, and electrophysiological features of Guillain-Barré syndrome in humans. However, the molecular pathogenesis of EAN remains controversial. Therefore, for this study, we induced EAN with P0 protein peptide 180-199 in CD4(-/-), CD8(-/-), CD4(-)8(-), and B cell knockout (microMT) mice to further investigate the roles of these cells in EAN. Our results showed that the severity of clinical signs and histopathological manifestations of EAN and the T cell response to P0 peptide 180-199 in CD4(-/-) mice were significantly lower than those in their wild-type counterparts. CD8(-/-) mice also had a milder clinical course, less histopathological change, and a diminished T cell response to P0 peptide 180-199. However, more severe clinical and histopathological manifestations, a stronger T cell response to P0 peptide 180-199, and enhanced IFN-gamma production in the spleen were observed in the EAN of CD4(-)8(-) and microMT mice, but these were not obviously different from those of wild-type mice. Levels of IgG production were similar in sera from CD4(-/-), CD8(-/-), and CD4(-)8(-), and wild-type mice. These findings suggest that the induction and control of murine EAN are dependent on both CD4(+) and CD8(+) T cells and that B cells apparently do not perpetuate the related inflammatory demyelination.

Animals↗
PubMed1998

Clomipramine and imipramine suppress clinical signs and T and B cell response to myelin proteins in experimental autoimmune neuritis in Lewis rats.

5-Hydroxytryptamine (5-HT) reuptake inhibitors of the zimeldine-type have induced polyneuropathies similar to Guillain-Barré syndrome (GBS) in patients with endogenous depression. Some monoamine neurotransmitters have been shown to affect immune reactions in vivo and in vitro in a concentration-dependent manner. We therefore studied the effect of the monoamine reuptake inhibitory anti-depressants, clomipramine and imipramine on specific immune response and the clinical course of experimental autoimmune neuritis (EAN), the animal model of GBS in humans. Clomipramine and imipramine both suppressed clinical signs of EAN induced by immunization with bovine peripheral nerve myelin (BPM), when given at a dose of 20 mg/kg/day intraperitoneally, via osmotic pumps. Clomipramine and imipramine reduced the numbers of Th1 cells secreting IFN-gamma in response to the neuritogenic myelin proteins BPM, P0 and P2 among lymph node mononuclear cells (MNC) from rats with EAN. The levels of cells secreting IgG antibodies to BPM, P2 and GM1 in lymph nodes were reduced at the height of EAN in clomipramine and imipramine treated animals. The action of clomipramine and imipramine on induced IFN-gamma and anti-myelin antibodies suggests that the mechanism for the suppressive effect of those substances on EAN symptoms may be due to an action on myelin T and B cell autoreactivity. Considering that the main common pharmacological principle of clomipramine and imipramine is to increase the functional activity of the nor-adrenaline (NA) and serotonin (5-HT) of the monoamines, it seems justified to postulate that the actions of clomipramine and imipramine demonstrated in this study to some extent involve NA and/or 5-HT. The immunomodulatory effects of clomipramine and imipramine call for further research on the potential role of drugs acting on the monoamine system in the treatment of autoimmune diseases, and for further studies of immunological mechanisms in the pathogenesis of depressive disorders.

Adrenergic Uptake Inhibitors↗
PubMed1999

Nasal administration of recombinant rat IL-4 ameliorates ongoing experimental autoimmune neuritis and inhibits demyelination.

Experimental autoimmune neuritis (EAN) is a CD4(+)T cell-mediated demyelinating disease of the peripheral nervous system (PNS) and serves as an experimental model for human immune-demyelinating neuropathies. In this study, we examined the effect of recombinant rat interleukin-4 (rrIL-4) on chronic EAN in Lewis rats induced by immunization with P0 peptide 180-199 and complete Freund's adjuvant (CFA). We estimated that nasal administration of rrIL-4, in dose ranges of 0.1-1 microg/rat/day in the initial phase of EAN, decreased the severity and the duration of clinical EAN. Hyporesponsiveness of T cells, downregulation of Th1 cell responses (INF-gamma), but increased levels of specific IgG1 isotypes document that nasal administration of rrIL-4 was systemically immune effective. Low grade inflammation and complete lack of regional demyelination within the sciatic nerves were seen in rrIL-4 treated rats. Based on these observations we suggest that nasal administration of IL-4 could be further evaluated, considering its possible use in human immune-demyelinating neuropathies.

Administration, Intranasal↗
PubMed1999

Amelioration of experimental allergic neuritis by sodium fusidate (fusidin): suppression of IFN-gamma and TNF-alpha and enhancement of IL-10.

The immunomodulating antibiotic drug fusidic acid and its sodium salt sodium fusidate (fusidin) ameliorate several organ-specific immunoinflammatory diseases. Because preliminary observations suggest that fusidin may also exert a beneficial effect in Guillain-Barré syndrome (GBS), here we have studied the effects of fusidin on actively induced experimental autoimmune neuritis (EAN) in rats, a known animal model for GBS. Both prophylactic and therapeutic treatment with fusidin (4 mg/rat day ip) markedly ameliorated the clinical course of the disease compared to vehicle-treated animals. The beneficial effects were associated with profound modifications of the capacity of these rats to produce and release pro- and anti-inflammatory cytokines such as IFN-gamma, TNF-alpha and IL-10, which are important in regulating the development of EAN.

Animals↗
PubMed1990

Central fiber contribution to W-shaped visual evoked potentials in patients with optic neuritis.

We studied W-shaped waveforms that occurred in full-field responses to pattern large-field stimulation in patients who had optic neuritis. Affected eyes showed no absolute scotomata; visual acuity was normal at the time of recording. To evaluate the contribution of macular- and paramacular-derived components to the development of the W-shaped waveforms in the patients, half-field and central full-field stimulation was used. The responses were compared with those obtained with the use of experimental scotomata in healthy subjects. The W-shaped waveforms recorded in the patients closely resembled the responses observed in healthy subjects after the introduction of experimental scotomata. In all affected eyes, half-field stimulation showed absence of the ipsilateral P100 component or its interaction with the P135 component. Enhanced paramacular N105 and P135 components were seen over the contralateral hemisphere. Responses to central full-field stimulation were an attenuated and prolonged P100 in the majority of affected eyes. Results of our study showed that W-shaped waveforms in response to large full-field stimulation may reflect impaired function of macular fibers. These electrophysiologic findings, however, were not always associated with evidence of a central field defect demonstrated by Friedmann perimetry.

Adolescent↗