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Article ; Online: Tryptophan Catabolites and Their Impact on Multiple Sclerosis Progression.

Watzlawik, Jens O / Wootla, Bharath / Rodriguez, Moses

2016 Volume 22, Issue 8, Page(s) 1049–1059

Abstract: Accumulating evidence demonstrates involvement of tryptophan metabolites and in particular activation of the kynurenine pathway (KP) in neurocognitive disorders under CNS inflammatory conditions. The KP is involved in several brain-associated disorders ... ...

Abstract	Accumulating evidence demonstrates involvement of tryptophan metabolites and in particular activation of the kynurenine pathway (KP) in neurocognitive disorders under CNS inflammatory conditions. The KP is involved in several brain-associated disorders including Parkinson's disease, AIDS dementia, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, schizophrenia, and brain tumors. Our review is an attempt to address any relevant association between dysregulation of KP and multiple sclerosis (MS), an inflammatory CNS disorder that ultimately leads to demyelinated brain areas and severe neurological deficits. Modulation of KP is a new topic for the field of MS and warrants further research. The availability of potential KP modulators approved for MS may shed some light into the therapeutic potential of KP antagonists for the treatment of MS patients.
MeSH term(s)	Animals ; Disease Progression ; Humans ; Multiple Sclerosis/physiopathology ; Tryptophan/metabolism
Chemical Substances	Tryptophan (8DUH1N11BX)
Language	English
Publishing date	2016
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Multiple Sclerosis, Gut Microbiota and Permeability: Role of Tryptophan Catabolites, Depression and the Driving Down of Local Melatonin.

Rodriguez, Moses / Wootla, Bharath / Anderson, George

Current pharmaceutical design

2016 Volume 22, Issue 40, Page(s) 6134–6141

Abstract: Background: Alterations in gut microbiota, coupled to increased gut permeability are now widely recognized as having a role in the etiology, course and treatment of many medical conditions, including autoimmune and neurodegenerative disorders.: ... ...

Abstract	Background: Alterations in gut microbiota, coupled to increased gut permeability are now widely recognized as having a role in the etiology, course and treatment of many medical conditions, including autoimmune and neurodegenerative disorders. Methods: In this review, the role that such gut changes play over the course of multiple sclerosis (MS) is detailed. Results: Given the wide array of biological factors and processes that have been shown to be altered in MS, including changes in the gut, this allows for a better integration of the diverse array of pathophysiological processes linked to MS. Such pathophysiological processes include increases in oxidative and nitrosative stress, pro-inflammatory immune responses, especially T helper (Th)17 cell proliferation and activation, tryptophan catabolites, pain, fatigue and increased levels of depression. By raising levels of immune activation, increased gut permeability and alterations in gut microbiota impact on all of these MS-associated processes. Alterations in the regulation of local melatonergic pathway activation is proposed to be an important hub for such pathophysiological processes in MS, allowing for the increased frequency of depression that may be prodromal in MS, both in the first episode as well as in relapses, to become more intimately associated with the etiology and course of MS. We propose this occurs by decreasing serotonin availability as a precursor for the melatoninergic pathways. Conclusion: Changes in the gut are evident in the early stages of MS, including in paediatric MS, and may interact with pro-inflammatory genetic susceptibility genes to drive the biological underpinnings of MS. Such a conceptualization of the biological underpinnings of MS also has treatment implications.
MeSH term(s)	Animals ; Depression/metabolism ; Gastrointestinal Microbiome/immunology ; Humans ; Melatonin/metabolism ; Multiple Sclerosis/immunology ; Multiple Sclerosis/metabolism ; Permeability ; Tryptophan/metabolism
Chemical Substances	Tryptophan (8DUH1N11BX) ; Melatonin (JL5DK93RCL)
Language	English
Publishing date	2016-07-01
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/1381612822666160915160520
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Article ; Online: Tryptophan Metabolites and Their Impact on Multiple Sclerosis Progression.

Watzlawik, Jens O / Wootla, Bharath / Rodriguez, Moses

Current pharmaceutical design

2015

Abstract	Accumulating evidence demonstrates involvement of tryptophan metabolites and in particular activation of the kynurenine pathway (KP) in neurocognitive disorders under CNS inflammatory conditions. The KP is involved in several brain-associated disorders including Parkinson's disease, AIDS dementia, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, schizophrenia, and brain tumors. Our review is an attempt to address any relevant association between dysregulation of KP and multiple sclerosis (MS), an inflammatory CNS disorder that ultimately leads to demyelinated brain areas and severe neurological deficits. Modulation of KP is a new topic for the field of MS and warrants further research. The availability of potential KP modulators approved for MS may shed some light into the therapeutic potential of KP antagonists for the treatment of MS patients.
Language	English
Publishing date	2015-12-14
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: A human anti-polysialic acid antibody as a potential treatment to improve function in multiple sclerosis patients.

Watzlawik, Jens O / Painter, Meghan M / Wootla, Bharath / Rodriguez, Moses

Journal of nature and science

2016 Volume 1, Issue 8

Abstract: We previously identified a human monoclonal antibody, termed HIgM12 that stimulates spontaneous locomotor activity in a chronically demyelinating mouse model of multiple sclerosis. When tested as a molecular substrate, HIgM12 stimulated neurite ... ...

Abstract	We previously identified a human monoclonal antibody, termed HIgM12 that stimulates spontaneous locomotor activity in a chronically demyelinating mouse model of multiple sclerosis. When tested as a molecular substrate, HIgM12 stimulated neurite outgrowth
Language	English
Publishing date	2016-07-01
Publishing country	United States
Document type	Journal Article
ISSN	2377-2700
ISSN	2377-2700
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Article: Deletion of Virus-specific T-cells Enhances Remyelination in a Model of Multiple Sclerosis.

Denic, Aleksandar / Wootla, Bharath / Zoecklein, Laurie / Rodriguez, Moses

Journal of neurology & translational neuroscience

2014 Volume 2, Issue 1

Abstract: We used transgenic expression of capsid antigens to Theiler's murine encephalomyelitis virus (TMEV) to study how the immune response to VP1 and VP2 influences spinal cord demyelination, remyelination and axonal loss during the acute and chronic phases of ...

Abstract	We used transgenic expression of capsid antigens to Theiler's murine encephalomyelitis virus (TMEV) to study how the immune response to VP1 and VP2 influences spinal cord demyelination, remyelination and axonal loss during the acute and chronic phases of infection. Expression from birth of capsid antigen under the ubiquitin promoter resulted in tolerance to the antigen and absence of an immune response to the respective capsid antigen following virus infection. The transgenic mice were crossed to B10.Q mice normally susceptible to demyelination but which, when compared to FVB mice of the same H2
Language	English
Publishing date	2014-09-05
Publishing country	United States
Document type	Journal Article
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Article: Concomitant Use of Neuroprotective Drugs in Neuro Rehabilitation of Multiple Sclerosis.

Dasari, Harika / Wootla, Bharath / Warrington, Arthur E / Rodriguez, Moses

International journal of physical medicine & rehabilitation

2016 Volume 4, Issue 4

Abstract: We provide an overview of rehabilitation in neurological diseases. A large amount of literature available on neurorehabilitation is based from the rehabilitative work on stroke and spinal cord injuries. After a brief description of rehabilitation, the ... ...

Abstract	We provide an overview of rehabilitation in neurological diseases. A large amount of literature available on neurorehabilitation is based from the rehabilitative work on stroke and spinal cord injuries. After a brief description of rehabilitation, the potential application of neurorehabilitation in neurodegenerative diseases specifically multiple sclerosis (MS) is summarized. Since MS causes a wide variety of symptoms, the rehabilitation in MS patients may benefit from an interdisciplinary approach that encloses physiotherapy, cognitive rehabilitation, psychological therapy, occupational therapy, and other methods to improve fatigue. Neurorehabilitation helps patients to reach and maintain their optimal physical, psychological and intellectual, levels but it does not reverse long-term disabilities that arise from neurological disorders. This calls for the need of better neuroregenerative and neuroprotective treatment strategies in addition to neurorehabilitation. We discuss neuroprotective drugs aimed at preventing axonal, neuronal, myelin and oligodendrocyte damage and cell death that are approved and others that are currently in clinical trials, with an emphasis on human derived natural antibodies with remyleination potential. Our investigative group developed recombinant natural human IgM antibodies against oligodendrocytes and neurons with a potential for CNS repair and remyleination. One such recombinant antibody, rHIgM22 completed a phase 1 clinical trial with no toxicity and with an objective of promoting remyleination in multiple sclerosis. Inclusion of these drugs as a multifaceted approach may further enhance the efficacy of neurorehabilitation in neuroinflammatory and neurodegenerative disorders.
Language	English
Publishing date	2016-06-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2759326-5
ISSN	2329-9096
ISSN	2329-9096
DOI	10.4172/2329-9096.1000348
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A monoclonal natural human IgM protects axons in the absence of remyelination.

Wootla, Bharath / Denic, Aleksandar / Warrington, Arthur E / Rodriguez, Moses

Journal of neuroinflammation

2016 Volume 13, Issue 1, Page(s) 94

Abstract: Background: Whereas demyelination underlies early neurological symptoms in multiple sclerosis (MS), axonal damage is considered critical for permanent chronic deficits. Intracerebral infection of susceptible mouse strains with Theiler's murine ... ...

Abstract	Background: Whereas demyelination underlies early neurological symptoms in multiple sclerosis (MS), axonal damage is considered critical for permanent chronic deficits. Intracerebral infection of susceptible mouse strains with Theiler's murine encephalomyelitis virus (TMEV) results in chronic induced demyelinating disease (TMEV-IDD) with progressive axonal loss and neurologic dysfunction similar to progressive forms of MS. We previously reported that treatment of chronic TMEV-IDD mice with a neurite outgrowth-promoting natural human antibody, HIgM12, improved brainstem NAA concentrations and preserved functional motor activity. In order to translate this antibody toward clinical trial, we generated a fully human recombinant form of HIgM12, rHIgM12, determined the optimal in vivo dose for functional improvement in TMEV-IDD, and evaluated the functional preservation of descending spinal cord axons by retrograde labeling. Findings: SJL/J mice at 45 to 90 days post infection (dpi) were studied. A single intraperitoneal dose of 0.25 mg/kg of rHIgM12 per mouse is sufficient to preserve motor function in TMEV-IDD. The optimal dose was 10 mg/kg. rHIgM12 treatment protected the functional transport in spinal cord axons and led to 40 % more Fluoro-Gold-labeled brainstem neurons in retrograde transport studies. This suggests that axons are not only present but also functionally competent. rHIgM12-treated mice also contained more mid-thoracic (T6) spinal cord axons than controls. Conclusions: This study confirms that a fully human recombinant neurite outgrowth-promoting monoclonal IgM is therapeutic in a model of progressive MS using multiple reparative readouts. The minimum effective dose is similar to that of a remyelination-promoting monoclonal human IgM discovered by our group that is presently in clinical trials for MS.
MeSH term(s)	Animals ; Antibodies, Monoclonal/pharmacology ; Axons/drug effects ; Axons/pathology ; Brain Stem/pathology ; Disease Models, Animal ; Humans ; Immunoglobulin M/pharmacology ; Mice ; Multiple Sclerosis/pathology ; Neuroprotective Agents/pharmacology ; Spinal Cord/pathology ; Theilovirus
Chemical Substances	Antibodies, Monoclonal ; Immunoglobulin M ; Neuroprotective Agents
Language	English
Publishing date	2016-04-28
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1742-2094
ISSN (online)	1742-2094
DOI	10.1186/s12974-016-0561-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Polyclonal and monoclonal antibodies in clinic.

Wootla, Bharath / Denic, Aleksandar / Rodriguez, Moses

Methods in molecular biology (Clifton, N.J.)

2014 Volume 1060, Page(s) 79–110

Abstract: Immunoglobulins (Ig) or antibodies are heavy plasma proteins, with sugar chains added to amino-acid residues by N-linked glycosylation and occasionally by O-linked glycosylation. The versatility of antibodies is demonstrated by the various functions that ...

Abstract	Immunoglobulins (Ig) or antibodies are heavy plasma proteins, with sugar chains added to amino-acid residues by N-linked glycosylation and occasionally by O-linked glycosylation. The versatility of antibodies is demonstrated by the various functions that they mediate such as neutralization, agglutination, fixation with activation of complement and activation of effector cells. Naturally occurring antibodies protect the organism against harmful pathogens, viruses and infections. In addition, almost any organic chemical induces antibody production of antibodies that would bind specifically to the chemical. These antibodies are often produced from multiple B cell clones and referred to as polyclonal antibodies. In recent years, scientists have exploited the highly evolved machinery of the immune system to produce structurally and functionally complex molecules such as antibodies from a single B clone, heralding the era of monoclonal antibodies. Most of the antibodies currently in the clinic, target components of the immune system, are not curative and seek to alleviate symptoms rather than cure disease. Our group used a novel strategy to identify reparative human monoclonal antibodies distinct from conventional antibodies. In this chapter, we discuss the therapeutic relevance of both polyclonal and monoclonal antibodies in clinic.
MeSH term(s)	Animals ; Antibodies/immunology ; Antibodies/therapeutic use ; Antibodies, Monoclonal/immunology ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Humanized/immunology ; Antibodies, Monoclonal, Humanized/therapeutic use ; Humans ; Immunoglobulins, Intravenous/immunology ; Immunoglobulins, Intravenous/therapeutic use
Chemical Substances	Antibodies ; Antibodies, Monoclonal ; Antibodies, Monoclonal, Humanized ; Immunoglobulins, Intravenous
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-62703-586-6_5
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Emergence of antibodies endowed with proteolytic activity against High-mobility group box 1 protein (HMGB1) in patients surviving septic shock.

Barnay-Verdier, Stéphanie / Borde, Chloé / Fattoum, Lakhdar / Wootla, Bharath / Lacroix-Desmazes, Sébastien / Kaveri, Srini / Gibot, Sébastien / Maréchal, Vincent

Cellular immunology

2019 Volume 347, Page(s) 104020

Abstract: High-mobility group box 1 (HMGB1) concentration in serum or plasma has been proposed as an important biological marker in various inflammation-related pathologies. We previously showed that low titer autoantibodies against HMGB1 could emerge during the ... ...

Abstract	High-mobility group box 1 (HMGB1) concentration in serum or plasma has been proposed as an important biological marker in various inflammation-related pathologies. We previously showed that low titer autoantibodies against HMGB1 could emerge during the course of sepsis. Importantly their presence was positively related with patients' survival. In this study, we focused on plasma samples from 2 patients who survived sepsis and exhibited high titer antibodies to HMGB1. These antibodies were proved to be specific for HMGB1 since they did not bind to HMGB2 or to human serum albumin. Following IgG purification, it has shown that both patients secreted HMGB1-hydrolyzing autoantibodies in vitro. These findings suggested that proteolytic antibodies directed against HMGB1 can be produced in patients surviving septic shock.
MeSH term(s)	Autoantibodies/blood ; Autoantibodies/immunology ; HMGB1 Protein/immunology ; HMGB2 Protein/immunology ; Humans ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Proteolysis ; Serum Albumin, Human/immunology ; Shock, Septic/immunology ; Shock, Septic/mortality ; Shock, Septic/pathology
Chemical Substances	Autoantibodies ; HMGB1 Protein ; HMGB1 protein, human ; HMGB2 Protein ; Immunoglobulin G ; Serum Albumin, Human (ZIF514RVZR)
Language	English
Publishing date	2019-11-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80094-6
ISSN	1090-2163 ; 0008-8749
ISSN (online)	1090-2163
ISSN	0008-8749
DOI	10.1016/j.cellimm.2019.104020
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Article ; Online: Treatment with a recombinant human IgM that recognizes PSA-NCAM preserves brain pathology in MOG-induced experimental autoimmune encephalomyelitis.

Lemus, Hernan Nicolas / Warrington, Arthur E / Denic, Aleksandar / Wootla, Bharath / Rodriguez, Moses

Human antibodies

2017 Volume 25, Issue 3-4, Page(s) 121–129

Abstract: A single peripheral dose of CNS-binding IgMs promote remyelination and preserve axons in a number of animal models of neurologic disease. A myelin-binding recombinant human IgM (rHIgM22) is presently in a safety trial in MS patients following an acute MS ...

Abstract	A single peripheral dose of CNS-binding IgMs promote remyelination and preserve axons in a number of animal models of neurologic disease. A myelin-binding recombinant human IgM (rHIgM22) is presently in a safety trial in MS patients following an acute MS exacerbation. rHIgM22 (directed against oligodendrocytes) or rHIgM12 (directed against neurons) were administered to mice with MOG-induced experimental autoimmune encephalomyelitis (EAE) with study endpoints: clinical deficits and brain and spinal cord pathology. IgMs were administered at a therapeutic dose of 100 μ g intra peritoneal at the time of immunization (day -1, 0, +$1), disease onset (15 days) or peak of the disease (28 days). Disease course was not worsened by either human IgM regardless of the time of treatment. Of note, the human IgM that recognizes a carbohydrate epitope on gangliosides and NCAM, rHIgM12, reduced brain pathology when given at time of immunization or at onset of disease, but did not reduce clinical deficits or spinal cord disease burden. Hence, treatment with rHIgM12 resulted in marked reduction in meningeal inflammation. Data consistent with the hypothesis that in the EAE model this molecule has an immune-modulatory effect. Treatment with an anti-CD4 blocking IgG prevented both clinical course and CNS pathology. This pre-clinical study further supports the safety of therapeutic CNS-binding human IgMs in the presence of autoimmunity and clearly differentiates them from IgGs directed against MOG or aquaporin-4 that worsen neurologic disease.
Language	English
Publishing date	2017
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1383468-x
ISSN	1875-869X ; 1093-2607
ISSN (online)	1875-869X
ISSN	1093-2607
DOI	10.3233/HAB-170313
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