CovidV1, Istex, Corpus, bibRecord, 000333

Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination

Identifieur interne : 000333 ( Istex/Corpus ); précédent : 000332; suivant : 000334

Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination

Auteurs : Baziel Gm Van Engelen ; Kevin D. Pavelko ; Moses Rodriguez

Source :

Multiple Sclerosis [ 1352-4585 ] ; 1997-04.

RBID : ISTEX:D820B4F9C884EC54416F170F93E304A5D10AD254

English descriptors

Teeft :
- Albumin concentration, Animal model, Arch neurol, Autoantibody, Beneficial effect, Cerebrospinal fluid, Clinical improvement, Control group, Delta increase, Demyelinating, Demyelination, Experimental demyelination, Experimental models, Full remyelination, Immune, Immune model, Immune response, Immune system, Immunoglobulin, Ivig, Ivig administration, Ivig treatment, Lysolecithin model, Mayo clinic, Monoclonal antibody, Multiple sclerosis, Myelin, Myelin repair, Neurol, Normal mice, Normal polyclonal, Optic neuritis, Passive transfer, Pathogenic role, Physiological role, Polyclonal, Remyelination, Rodriguez, Sclerosis, Sodium channels, Spinal cord, Spontaneous remyelination, System remyelination, Tmev, Tmev model, Virus model.

Abstract

Studies in both humans and experimental animals indicate that there is potential for full remyelination following CNS demyelination, but the factors that control the degree of myelin repair are unknown. In the Theiler's virus model of demyelination CNS remyelination can be promoted either by global immunosuppression or by selective immunoglobulin therapy. In this paper we discuss whether immunoglobulin-mediated remyelination is a characteristic of immune-mediated demyelination, or whether immunoglobulin-mediated remyelination also occurs in the toxic-traumatic model of lysolecithin-induced demyelination. Our data support the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair.

Url:

https://api.istex.fr/ark:/67375/M70-3GCWK6L8-0/fulltext.pdf

DOI: 10.1177/135245859700300203

Links to Exploration step

ISTEX:D820B4F9C884EC54416F170F93E304A5D10AD254

Le document en format XML

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<meta-value>76 Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination SAGE Publications, Inc.1997DOI: 10.1177/135245859700300203 Baziel GM van Engelen Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA Immunology, Mayo Clinic, Rochester, Minnesota, USA Institute of Neurology, University Hospital Nijmegen, The Netherlands Kevin D Pavelko Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA Immunology, Mayo Clinic, Rochester, Minnesota, USA Moses Rodriguez Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA Immunology, Mayo Clinic, Rochester, Minnesota, USA Correspondence: BGM van Engelen Studies in both humans and experimental animals indicate that there is potential for full remyelination following CNS demyelination, but the factors that control the degree of myelin repair are unknown. In the Theiler's virus model of demyelination CNS remyelination can be promoted either by global immunosuppression or by selective immunoglobulin therapy. In this paper we discuss whether immunoglobulin-mediated remyelination is a characteristic of immune-mediated demyelination, or whether immunoglobulin-mediated remyelination also occurs in the toxic-traumatic model of lysolecithin-induced demyelination. Our data support the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair. remyelination demyelination CNS experimental models humans immunoglobulin Introduction Three general categories of experimentally-induced CNS demyelination can be distinguished: (1) toxin- induced [Cuprizone,' ethidium bromide 2 lysolewithin]3 (2) autoimmune-induced [experimental autoimmune encephalomyelitis (EAE)],' and (3) virus- induced [corona virus,' Theiler's murine encephalomyelitis virus (TMEV)].' Spontaneous CNS remyelination has been described in each of these experimental models of demyelination in rodents. There is also evidence that some CNS lesions of multiple sclerosis (MS) are remyelinated by oligodendrocytes7.8 or Schwann cells.9 However, most MS lesions examined at autopsy show extensive demyelination and gliosis without significant remyelination. These observations suggest that there is potential for full remyelination following episodes of demyelination in relapsing demyelinating diseases, but the factors that control the degree of remyelination are unknown. In the experimental model of demyelination induced by TMEV, a natural enteric picornavirus in mice, CNS remyelination can be promoted either by immunosuppression,'° or by immunostimulation by passive transfer of immunoglobulins such as CNS-specific antiserum," purified immunoglobulin,6 polyclonal mouse IgG,12 and a monoclonal autoantibody (mAb) designated SCH 94.03. 13 Such a beneficial effect of immunoglobulins is not merely a characteristic of the TMEV model, as Achiron et al'4 reported that polyclonal human IgG (IVIg) inhibits the active induction of EAE. In this paper we discuss whether IgG-mediated remyelination is a characteristic of immune-mediated demyelination, or whether IgG-mediated remyelination is a more general biological mechanism of myelin repair. We will review (i) the role and significance of oligoclonal IgG in MS, (ii) the effect of pooled immunoglobulins from normal non-syngeneic mice on CNS remyelination in the Theiler's virus model of demyelination, (iii) the results of a pilot-study on the potential of IVIg to promote remyelination in humans, and (iv) the passage of IgG through the blood- cerebrospinal fluid (CSF) barrier. Finally we discuss the possibility that even in a non-primary immune model of demyelination, immunomodulation is beneficial in myelin repair, by investigating (v) IgG-mediated remyelination in the toxic-traumatic model of lysolecithin-induced demyelination. The role and significance of oligoclonal IgG in MS A hallmark laboratory finding in MS is increased levels of IgG in the CSF. Decades of research have failed to show either the specificity of this oligoclonal IgG, or its function, which is generally assumed to be pathogenic.15 The presumed pathogenic role of IgG in MS needs to be reevaluated based on the discovery that certain autoantibodies are beneficial in an animal model of CNS demyelination6,13 and on theoretical grounds." The specificity of the oligoclonal immunoglobulin in CSF and MS lesions remains undetermined ; their pathogenicity has not been proved despite extensive investigation.15 In tissue cultures, the major demyelinating factor of MS serum seems to be a component other than IgG.'6 Intrathecal IgG synthesis occurs in patients with other neurological diseases (even in normal subjects) and no correlation exists between levels of intrathecal IgG synthesis and the progression of MS.17-20 Direct transfer of intrathecal IgG from MS patients or from animals with EAE fails to induce demyelination in recipient animals." In contrast, immunization with myelin components in animals with EAE have been shown to induce oligodendroglia proliferation, and to inhibit the development of EAE.2' From these experimental and clinical data the traditional notion of the immune response (in 77 particular IgG) solely as deleterious involved in the pathogenesis of demyelinating diseases like MS should be reconsidered. Intrathecal IgG synthesis may function as a marker of a stimulated immune response, or may represent an immune response secondary to myelin breakdown playing a physiological role in the catabolism of endogenous substances." A certain proportion of the oligoclonal CSF IgG in MS may belong to the large family of naturally occurring autoantibodies,22 and may be involved in promoting CNS remyelination similar to the autoreactive antibodies (autoantibodies against spinal cord homogenate) in the TMEV model of demyelination.'," Therefore the elevated IgG may reflect an attempt at immunological homeostasis, which implies that autoimmune diseases, and possibly also MS may be treated successfully not by suppressing the immune network, but by strengthening it by administration of IVIg. This suggestion agrees with the frequent association of autoimmunity with immunodeficiency.23 The effect of pooled immunoglobulins from normal non-syngeneic mice on CNS remyelination in the Theiler's virus model of demyelination Although antibodies can induce demyelination in vitro" as well as in vivo,25 they have also been shown to promote remyelination in experimental demyelination. Antibody-mediated oligodendrocyte stimulation has also been reported in vitro.26.27 Analogous in vivo treatment experiments were carried out in the TMEV model of demyelination. TMEV, a picorna virus, causes a chronic progressive immune-mediated CNS demyelinating disease similar pathologically and clinically to the chronic progressive form of MS. Passive transfer of CNS-specific antiserum," and purified immunoglobulin6.28 promoted CNS remyelination. In contrast to the classical view of the humoral immune system playing a pathogenic role in CNS demyelination, these experiments indicated for the first time that immunoblobulins, and in particular autoreactive immunoglobulins, i.e. autoantibodies, might play a beneficial role by promoting CNS remyelination. To further bridge the gap between the experimental and human studies we examined the effect of commercially available polyclonal IgG (Sigma Co., St. Louis MO, product no. 1-5381) prepared from non-syngeneic donor mice on TMEV-induced demyelination in SJL/J mice. The effect on remyelination by this product (dose 0.1 mg each week over 5 weeks administered intravenously) which is analogous to the human IVIg preparation was measured by quantitative morphometry as described earlier.' As controls we used SJL/J mice treated with borate buffered saline. There were three to five times more lesions with remyelination in the polyclonal IgG-treated group than in mice receiving the control treatment. In addition, the total area of CNS-type remyelination in mice receiving polyclonal IgG was six to 30 times that of the control mice. The difference between the polyclonal IgG group and the control group in the percentage of demyelinated area that showed remye- lination was statistically significant (P< 0.05). The extent of CNS remyelination observed following treatment with normal polyclonal IgG was similar to the extent of remyelination observed following treatment with CNS-specific immunoglobulins.6.28 If the mechanism of remyelination is mediated by CNS-specific autoantibodies, then this would imply that these autoantibodies were present in the normal polyclonal commercially available IgG preparation, as has in fact been shown by others for IgG isolated from pools of normal sera from various mouse strains.2n Of interest is, despite the differences in route and dose, that pooled polyclonal IgG from normal non-syngeneic mice promoted remyelination, while this was not the case in mice receiving IgG obtained from syngeneic SJL/J mice immunized with incomplete Freunds adjuvant or mice immunized with phosphate buffered saline." We hypothesize that there is a broader repertoire of antibodies (some with remyelinating potential) in the pooled polyclonal IgG from normal mice than in the laboratory-prepared IgG from the inbred strain of SJL/J mice. These findings increase the likelihood that human IVIg (non-syngeneic with multiple specificities) may also promote remyelination in human demyelinating diseases like MS. The results of a pilot-study on the potential of IVIG to promote remyelination in humans In view of this effect of antibodies mediating remyelination in an established experimental model of MS, we tested the potential of IVIg treatment to promote remyelination in MS in an open-label, unblinded study.3° In this open label study of five MS patients with non-recovering, static, optic neuritis eight eyes; optic neuritis duration 7 months to 4 years), the repeated administration of IVIg was followed within 1 or 2 months by improvement of visual acuity and color vision (five eyes), light brightness (three eyes), and visual evoked responses (five eyes). Improvement was temporally related to the administration of IVIg and has persisted for the follow-up period of 1.2 to 1.7 years. These findings suggest that IVIg administration in patients with non-recovering, steroid-unresponsive optic neuritis due to MS is associated with improvement of neurological function. The clinical improvement may have been due to IVIg- mediated promotion of remyelination, like the immunoglobulin-induced remyelination in the TMEV model of MS. The timing of the onset of clinical improvement (1- 2 months) was similar to the time course for spontaneous remyelination1.31.32 and for antibody-mediated remyelination.1 Alternatively, clinical improvement after IVIg may have occurred without morphological evidence of remyelination by an effect on optic nerve conductance. After demyelination, conduction can be restored by remyelination and by the re-establishment of saltatory conduction. Another possible mechanism of axon recovery after demyelination is continuous conduction. IVIg may have induced the capacity for optic nerves to conduct like unmyelinated fibers by the development of sodium channels in the internodal area. In this view IVIg may have stimulated a spontaneously occurring 78 adaptive repair mechanism in demyelinated fibers which has been reported in experimental demyelination and in patients with MS.33 The possible role of IVIg in restoring clinical function and promoting CNS remyelination needs to be confirmed with a larger, controlled trial. This pilot study was performed to determine if a more extended controlled and blinded study would be worthwhile. Two controlled trials testing IVIg in MS patients with severe functional motor deficits or visual loss from optic neuritis are underway at the Mayo Clinic. Human IVIg and the passage of IgG through the blood-CSF barrier Purpose of this study was to examine passage of IgG through the blood-CSF barrier and to elucidate mechanisms of action and adverse effects of IVIg. IVIg was administered in a booster dose of 0.4 gm/kg body weight per day for 5 days, followed by the same dose once every 2 weeks during 3 months. Before and after administration of IVIg, CSF was examined in a homogeneous group of 15 patients with cryptogenic epilepsies (West syndrome and Lennox-Gastaut syndrome). Following IVIg administration in these patients, all with an on the whole undisturbed blood-CSF barrier permeability as measured by Q albumin (CSF albumin concentration x 105/serum albumin concentration). Serum total IgG and CSF IgG were increased significantly compared to the pretreatment values. Serum total IgG increased in all patients ranging from 5 to 186% (mean 76%). CSF IgG was elevated in all but one patient. The CSF IgG increase ranged from 22 to 89% (mean 44%). The delta increase in CSF IgG (=CSF IgG after treatment minus CSF IgG before treatment) ranged from 5 to 11 mg/L. The delta increase in CSF IgG correlated positively (p=0.9) with Q albumin (a measure of blood-CSF permeability). After IVIg, no increase of mononucleated cells indicative of an adverse reaction such as aseptic meningoencephalitis34 was found. As Q albumin in individual patients is a measure for the blood-CSF barrier permeability,35 a higher Q albumin should be associated with a higher IgG transfer from blood into CSF across the blood-CSF barrier. In these patients, all of whom had normal Q albumin levels, which indicates a generally undisturbed blood-CSF barrier permeability, IVIg treatment was able to increase CSF IgG. This is in accordance with the normal situation of transfer of IgG from blood to the CSF.36-38 IgG mediated remyelination in the toxic-traumatic model of lysolecithin-induced demyelination We studied whether the beneficial effect of manipulating the immune response is restricted to immune-mediated models (such as TMEV) or whether immunoglobulins and corticosteroids could promote remyelination in the well established toxic traumatic model of lysolecithin-induced non immune demyelination. The lysolecithin model enables to dissect in time a drug effect on demyelination and remyelination, which is impossible in a complex human disease with a highly variable course like MS. Drug administration followed the induction of demyelination in an attempt to mimic the clinical situation, where treatment is applied after myelin degradation has already begun. We first investigated spontaneous remyelination in phosphate buffered saline (PBS)-treated control mice, 2, 3 and 5 weeks after lysolecithin-induced demyelination in the spinal cord. The number of remyelinating axons per MM2 lesion increased significantly 3 and 5 weeks after lysolecithin injection. Methylprednisolone and a monoclonal antibody (mAb SCH 94.03)13.39 developed for its ability to promote remyelination in the Theiler's virus model of demyelination further increased spontaneous remyelination by a factor 3.2 and 2.6 respectively, but not the ratio of myelin sheath thickness to axon diameter or the number of proliferating cells in the lesion. After 3 weeks, the extent of remyelination in the methylprednisolone and mAb SCH 94.03 treatment groups was similar to the spontaneous remyelination in the 5 weeks PBS control group. This study extends our findings on the promotion of CNS remyelination in the Theiler's model of demyelination, and supports the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair. mAb SCH 94.03 has phenotypic characteristics of natural occurring or physiological autoantibodies, which are found in the serum of normal humans and mice, and are polyreactive with a wide range of antigens. mAb SCH 94.03 shows reactivity toward several protein antigens and chemical haptens, with prominent reactivity toward spectrin, and fluorescein; it is encoded by germline immunoglobulin light chain and heavy chain genes without definitive somatic mutations.38 Promotion of spontaneous remyelination in the lysolecithin model by a natural occurring autoantibody (mAb SCH 94.03) suggests that certain natural autoantibodies may participate in a beneficial physiological response to CNS injury, even in non- immune models of demyelination. 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<titleInfo type="alternative" lang="en" contentType="CDATA"><title>Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination</title>
</titleInfo>
<name type="personal"><namePart type="given">Baziel GM</namePart>
<namePart type="family">van Engelen</namePart>
<affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA, Immunology, Mayo Clinic, Rochester, Minnesota, USA, Institute of Neurology, University Hospital Nijmegen, The Netherlands</affiliation>
</name>
<name type="personal"><namePart type="given">Kevin D</namePart>
<namePart type="family">Pavelko</namePart>
<affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA, Immunology, Mayo Clinic, Rochester, Minnesota, USA</affiliation>
</name>
<name type="personal"><namePart type="given">Moses</namePart>
<namePart type="family">Rodriguez</namePart>
<affiliation>Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA, Immunology, Mayo Clinic, Rochester, Minnesota, USA</affiliation>
</name>
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<abstract lang="en">Studies in both humans and experimental animals indicate that there is potential for full remyelination following CNS demyelination, but the factors that control the degree of myelin repair are unknown. In the Theiler's virus model of demyelination CNS remyelination can be promoted either by global immunosuppression or by selective immunoglobulin therapy. In this paper we discuss whether immunoglobulin-mediated remyelination is a characteristic of immune-mediated demyelination, or whether immunoglobulin-mediated remyelination also occurs in the toxic-traumatic model of lysolecithin-induced demyelination. Our data support the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair.</abstract>
<subject><genre>keywords</genre>
<topic>remyelination</topic>
<topic>demyelination</topic>
<topic>CNS</topic>
<topic>experimental models</topic>
<topic>humans</topic>
<topic>immunoglobulin</topic>
</subject>
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<identifier type="eISSN">1477-0970</identifier>
<identifier type="PublisherID">MSJ</identifier>
<identifier type="PublisherID-hwp">spmsj</identifier>
<part><date>1997</date>
<detail type="volume"><caption>vol.</caption>
<number>3</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>2</number>
</detail>
<extent unit="pages"><start>76</start>
<end>79</end>
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Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination

Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination

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