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Article: Corrigendum: IgG2 rules: N-acetyl-β-D-glucosamine-specific IgG2 and Th17/Th1 cooperation may promote the pathogenesis of acute rheumatic heart disease and be a biomarker of the autoimmune sequelae of

Kirvan, Christine A / Canini, Heather / Swedo, Susan E / Hill, Harry / Veasy, George / Jankelow, David / Kosanke, Stanley / Ward, Kent / Zhao, Yan D / Alvarez, Kathy / Hedrick, Andria / Cunningham, Madeleine W

Frontiers in cardiovascular medicine

2023 Volume 10, Page(s) 1267920

Abstract: This corrects the article DOI: 10.3389/fcvm.2022.919700.]. ...

Abstract	[This corrects the article DOI: 10.3389/fcvm.2022.919700.].
Language	English
Publishing date	2023-08-31
Publishing country	Switzerland
Document type	Published Erratum
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2023.1267920
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Axolemmal nanoruptures arising from paranodal membrane injury induce secondary axon degeneration in murine Guillain-Barré syndrome.

Cunningham, Madeleine E / McGonigal, Rhona / Barrie, Jennifer A / Campbell, Clare I / Yao, Denggao / Willison, Hugh J

Journal of the peripheral nervous system : JPNS

2023 Volume 28, Issue 1, Page(s) 17–31

Abstract: The major determinant of poor outcome in Guillain-Barré syndrome (GBS) is axonal degeneration. Pathways leading to primary axonal injury in the motor axonal variant are well established, whereas mechanisms of secondary axonal injury in acute inflammatory ...

Abstract	The major determinant of poor outcome in Guillain-Barré syndrome (GBS) is axonal degeneration. Pathways leading to primary axonal injury in the motor axonal variant are well established, whereas mechanisms of secondary axonal injury in acute inflammatory demyelinating polyneuropathy (AIDP) are unknown. We recently developed an autoantibody-and complement-mediated model of murine AIDP, in which prominent injury to glial membranes at the node of Ranvier results in severe disruption to paranodal components. Acutely, axonal integrity was maintained, but over time secondary axonal degeneration occurred. Herein, we describe the differential mechanisms underlying acute glial membrane injury and secondary axonal injury in this model. Ex vivo nerve-muscle explants were injured for either acute or extended periods with an autoantibody-and complement-mediated injury to glial paranodal membranes. This model was used to test several possible mechanisms of axon degeneration including calpain activation, and to monitor live axonal calcium signalling. Glial calpains induced acute disruption of paranodal membrane proteins in the absence of discernible axonal injury. Over time, we observed progressive axonal degeneration which was markedly attenuated by axon-specific calpain inhibition. Injury was unaffected by all other tested methods of protection. Trans-axolemmal diffusion of fluorescent proteins and live calcium imaging studies indirectly demonstrated the presence of nanoruptures in the axon membrane. This study outlines one mechanism by which secondary axonal degeneration arises in the AIDP variant of GBS where acute paranodal loop injury is prominent. The data also support the development of calpain inhibitors to attenuate both primary and secondary axonal degeneration in GBS.
MeSH term(s)	Humans ; Mice ; Animals ; Guillain-Barre Syndrome ; Calcium ; Calpain ; Axons ; Autoantibodies
Chemical Substances	Calcium (SY7Q814VUP) ; Calpain (EC 3.4.22.-) ; Autoantibodies
Language	English
Publishing date	2023-02-12
Publishing country	United States
Document type	Case Reports ; Research Support, Non-U.S. Gov't
ZDB-ID	1364009-4
ISSN	1529-8027 ; 1085-9489
ISSN (online)	1529-8027
ISSN	1085-9489
DOI	10.1111/jns.12532
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Article: TGM6, a helminth secretory product, mimics TGF-β binding to TβRII to antagonize TGF-β signaling in fibroblasts.

White, Stephen E / Schwartze, Tristin A / Mukundan, Ananya / Schoenherr, Christina / Singh, Shashi P / van Dinther, Maarten / Cunningham, Kyle T / White, Madeleine P J / Campion, Tiffany / Pritchard, John / Hinck, Cynthia S / Ten Dijke, Peter / Inman, Gareth / Maizels, Rick M / Hinck, Andrew P

bioRxiv : the preprint server for biology

2023

Abstract: The murine helminth ... ...

Abstract	The murine helminth parasite
Language	English
Publishing date	2023-12-23
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.12.22.573140
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Article ; Online: Real time imaging of intra-axonal calcium flux in an explant mouse model of axonal Guillain-Barré syndrome.

Cunningham, Madeleine E / McGonigal, Rhona / Barrie, Jennifer A / Yao, Denggao / Willison, Hugh J

Experimental neurology

2022 Volume 355, Page(s) 114127

Abstract: The acute motor axonal variant of Guillain-Barré syndrome is associated with the attack of motor axons by anti-ganglioside antibodies which activate complement on the axonal plasma membrane. Animal models have indirectly implicated complement pore- ... ...

Abstract	The acute motor axonal variant of Guillain-Barré syndrome is associated with the attack of motor axons by anti-ganglioside antibodies which activate complement on the axonal plasma membrane. Animal models have indirectly implicated complement pore-mediated calcium influx as a trigger of axonal damage, through the activation of the protease calpain. However, this calcium influx has never been imaged directly. Herein we describe a method to detect changes in intra-axonal calcium in an ex vivo mouse model of axonal Guillain-Barré syndrome and describe the influence of calcium on axonal injury and the effects of calpain inhibition on axonal outcome. Using ex vivo nerve-muscle explants from Thy1-TNXXL mice which axonally express a genetically encoded calcium indicator, we studied the effect of the binding and activation of complement by an anti-GD1b ganglioside antibody which targets the motor axon. Using live multiphoton imaging, we found that a wave of calcium influx extends retrogradely from the motor nerve terminal as far back as the large bundles within the muscle explant. Despite terminal complement pores being detectable only at the motor nerve terminal and, to a lesser degree, the most distal node of Ranvier, disruption of axonal proteins occurred at more proximal sites implicating the intra-axonal calcium wave. Morphological analysis indicated two different types of calcium-induced changes: acutely, distal axons showed swelling and breakdown at sites where complement pores were present. Distally, in areas of raised calcium which lacked detectable complement pores, axons developed a spindly, vacuolated appearance suggestive of early signs of degeneration. All morphological changes were prevented with treatment with a calpain inhibitor. This is the first investigation of axonal calcium dynamics in a mouse model of Guillain-Barré syndrome and demonstrates the proximal reach of calcium influx following an injury which is confined to the most distal parts of the motor axon. We also demonstrate that calpain inhibition remains a promising candidate for both acute and sub-acute consequences of calcium-induced calpain activation.
MeSH term(s)	Animals ; Axons ; Calcium ; Calpain ; Complement System Proteins ; Disease Models, Animal ; Gangliosides ; Guillain-Barre Syndrome ; Mice
Chemical Substances	Gangliosides ; Complement System Proteins (9007-36-7) ; Calpain (EC 3.4.22.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-05-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2022.114127
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Article: IgG2 rules: N-acetyl-β-D-glucosamine-specific IgG2 and Th17/Th1 cooperation may promote the pathogenesis of acute rheumatic heart disease and be a biomarker of the autoimmune sequelae of

Frontiers in cardiovascular medicine

2023 Volume 9, Page(s) 919700

Abstract: Antecedent group A streptococcal pharyngitis is a well-established cause of acute rheumatic fever (ARF) where rheumatic valvular heart disease (RHD) and Sydenham chorea (SC) are major manifestations. In ARF, crossreactive antibodies and T cells respond ... ...

Abstract	Antecedent group A streptococcal pharyngitis is a well-established cause of acute rheumatic fever (ARF) where rheumatic valvular heart disease (RHD) and Sydenham chorea (SC) are major manifestations. In ARF, crossreactive antibodies and T cells respond to streptococcal antigens, group A carbohydrate, N-acetyl-β-
Language	English
Publishing date	2023-02-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2022.919700
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Article ; Online: Schwann cell nodal membrane disruption triggers bystander axonal degeneration in a Guillain-Barré syndrome mouse model.

McGonigal, Rhona / Campbell, Clare I / Barrie, Jennifer A / Yao, Denggao / Cunningham, Madeleine E / Crawford, Colin L / Rinaldi, Simon / Rowan, Edward G / Willison, Hugh J

The Journal of clinical investigation

2022 Volume 132, Issue 14

Abstract: In Guillain-Barré syndrome (GBS), both axonal and demyelinating variants can be mediated by complement-fixing anti-GM1 ganglioside autoantibodies that target peripheral nerve axonal and Schwann cell (SC) membranes, respectively. Critically, the extent of ...

Abstract	In Guillain-Barré syndrome (GBS), both axonal and demyelinating variants can be mediated by complement-fixing anti-GM1 ganglioside autoantibodies that target peripheral nerve axonal and Schwann cell (SC) membranes, respectively. Critically, the extent of axonal degeneration in both variants dictates long-term outcome. The differing pathomechanisms underlying direct axonal injury and the secondary bystander axonal degeneration following SC injury are unresolved. To investigate this, we generated glycosyltransferase-disrupted transgenic mice that express GM1 ganglioside either exclusively in neurons [GalNAcT-/--Tg(neuronal)] or glia [GalNAcT-/--Tg(glial)], thereby allowing anti-GM1 antibodies to solely target GM1 in either axonal or SC membranes, respectively. Myelinated-axon integrity in distal motor nerves was studied in transgenic mice exposed to anti-GM1 antibody and complement in ex vivo and in vivo injury paradigms. Axonal targeting induced catastrophic acute axonal disruption, as expected. When mice with GM1 in SC membranes were targeted, acute disruption of perisynaptic glia and SC membranes at nodes of Ranvier (NoRs) occurred. Following glial injury, axonal disruption at NoRs also developed subacutely, progressing to secondary axonal degeneration. These models differentiate the distinctly different axonopathic pathways under axonal and glial membrane targeting conditions, and provide insights into primary and secondary axonal injury, currently a major unsolved area in GBS research.
MeSH term(s)	Animals ; Autoantibodies ; Disease Models, Animal ; G(M1) Ganglioside ; Gangliosides ; Guillain-Barre Syndrome/genetics ; Mice ; Mice, Transgenic ; Schwann Cells
Chemical Substances	Autoantibodies ; Gangliosides ; G(M1) Ganglioside (37758-47-7)
Language	English
Publishing date	2022-06-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI158524
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Article ; Online: Complement inhibition prevents glial nodal membrane injury in a GM1 antibody-mediated mouse model.

Campbell, Clare I / McGonigal, Rhona / Barrie, Jennifer A / Delaere, Jolien / Bracke, Laura / Cunningham, Madeleine E / Yao, Denggao / Delahaye, Tim / Van de Walle, Inge / Willison, Hugh J

Brain communications

2022 Volume 4, Issue 6, Page(s) fcac306

Abstract: The involvement of the complement pathway in Guillain-Barré syndrome pathogenesis has been demonstrated in both patient biosamples and animal models. One proposed mechanism is that anti-ganglioside antibodies mediate neural membrane injury through the ... ...

Abstract	The involvement of the complement pathway in Guillain-Barré syndrome pathogenesis has been demonstrated in both patient biosamples and animal models. One proposed mechanism is that anti-ganglioside antibodies mediate neural membrane injury through the activation of complement and the formation of membrane attack complex pores, thereby allowing the uncontrolled influx of ions, including calcium, intracellularly. Calcium influx activates the calcium-dependent protease calpain, leading to the cleavage of neural cytoskeletal and transmembrane proteins and contributing to subsequent functional failure. Complement inhibition has been demonstrated to provide effective protection from injury in anti-ganglioside antibody-mediated mouse models of axonal variants of Guillain-Barré syndrome; however, the role of complement in the pathogenesis of demyelinating variants has yet to be established. Thus, it is currently unknown whether complement inhibition would be an effective therapeutic for Guillain-Barré syndrome patients with injuries to the Schwann cell membrane. To address this, we recently developed a mouse model whereby the Schwann cell membrane was selectively targeted with an anti-GM1 antibody resulting in significant disruption to the axo-glial junction and cytoplasmic paranodal loops, presenting as conduction block. Herein, we utilize this Schwann cell nodal membrane injury model to determine the relevance of inhibiting complement activation. We addressed the early complement component C2 as the therapeutic target within the complement cascade by using the anti-C2 humanized monoclonal antibody, ARGX-117. This anti-C2 antibody blocks the formation of C3 convertase, specifically inhibiting the classical and lectin complement pathways and preventing the production of downstream harmful anaphylatoxins (C3a and C5a) and membrane attack complexes. Here, we demonstrate that C2 inhibition significantly attenuates injury to paranodal proteins at the node of Ranvier and improves respiratory function in
Language	English
Publishing date	2022-11-23
Publishing country	England
Document type	Journal Article
ISSN	2632-1297
ISSN (online)	2632-1297
DOI	10.1093/braincomms/fcac306
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Article ; Online: The endogenous calpain inhibitor calpastatin attenuates axon degeneration in murine Guillain-Barré syndrome.

McGonigal, Rhona / Cunningham, Madeleine E / Smyth, Duncan / Chou, Michael / Barrie, Jennifer A / Wilkie, Andrew / Campbell, Clare / Saatman, Kathryn E / Lunn, Michael / Willison, Hugh J

Journal of the peripheral nervous system : JPNS

2022 Volume 28, Issue 1, Page(s) 4–16

Abstract: Axon degeneration accounts for the poor clinical outcome in Guillain-Barré syndrome (GBS), yet no treatments target this key pathogenic stage. Animal models demonstrate anti-ganglioside antibodies (AGAb) induce axolemmal complement pore formation through ...

Abstract	Axon degeneration accounts for the poor clinical outcome in Guillain-Barré syndrome (GBS), yet no treatments target this key pathogenic stage. Animal models demonstrate anti-ganglioside antibodies (AGAb) induce axolemmal complement pore formation through which calcium flux activates the intra-axonal calcium-dependent proteases, calpains. We previously showed protection of axonal components using soluble calpain inhibitors in ex vivo GBS mouse models, and herein, we assess the potential of axonally-restricted calpain inhibition as a neuroprotective therapy operating in vivo. Using transgenic mice that over-express the endogenous human calpain inhibitor calpastatin (hCAST) neuronally, we assessed distal motor nerve integrity in our established GBS models. We induced immune-mediated injury with monoclonal AGAb plus a source of human complement. The calpain substrates neurofilament and AnkyrinG, nerve structural proteins, were assessed by immunolabelling and in the case of neurofilament, by single-molecule arrays (Simoa). As the distal intramuscular portion of the phrenic nerve is prominently targeted in our in vivo model, respiratory function was assessed by whole-body plethysmography as the functional output in the acute and extended models. hCAST expression protects distal nerve structural integrity both ex and in vivo, as shown by attenuation of neurofilament breakdown by immunolabelling and Simoa. In an extended in vivo model, while mice still initially undergo respiratory distress owing to acute conduction failure, the recovery phase was accelerated by hCAST expression. Axonal calpain inhibition can protect the axonal integrity of the nerve in an in vivo GBS paradigm and hasten recovery. These studies reinforce the strong justification for developing further animal and human clinical studies using exogenous calpain inhibitors.
MeSH term(s)	Mice ; Humans ; Animals ; Guillain-Barre Syndrome ; Calpain/metabolism ; Calcium/metabolism ; Axons/pathology ; Mice, Transgenic
Chemical Substances	calpain inhibitors ; calpastatin (79079-11-1) ; Calpain (EC 3.4.22.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-11-18
Publishing country	United States
Document type	Case Reports ; Research Support, Non-U.S. Gov't
ZDB-ID	1364009-4
ISSN	1529-8027 ; 1085-9489
ISSN (online)	1529-8027
ISSN	1085-9489
DOI	10.1111/jns.12520
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Zs.A 5106: Show issues

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Article ; Online: Cerebellar deep brain stimulation for chronic post-stroke motor rehabilitation: a phase I trial.

Baker, Kenneth B / Plow, Ela B / Nagel, Sean / Rosenfeldt, Anson B / Gopalakrishnan, Raghavan / Clark, Cynthia / Wyant, Alexandria / Schroedel, Madeleine / Ozinga, John / Davidson, Sara / Hogue, Olivia / Floden, Darlene / Chen, Jacqueline / Ford, Paul J / Sankary, Lauren / Huang, Xuemei / Cunningham, David A / DiFilippo, Frank P / Hu, Bo /

Jones, Stephen E / Bethoux, Francois / Wolf, Steven L / Chae, John / Machado, André G

Nature medicine

2023 Volume 29, Issue 9, Page(s) 2366–2374

Abstract: Upper-extremity impairment after stroke remains a major therapeutic challenge and a target of neuromodulation treatment efforts. In this open-label, non-randomized phase I trial, we applied deep brain stimulation to the cerebellar dentate nucleus ... ...

Abstract	Upper-extremity impairment after stroke remains a major therapeutic challenge and a target of neuromodulation treatment efforts. In this open-label, non-randomized phase I trial, we applied deep brain stimulation to the cerebellar dentate nucleus combined with renewed physical rehabilitation to promote functional reorganization of ipsilesional cortex in 12 individuals with persistent (1-3 years), moderate-to-severe upper-extremity impairment. No serious perioperative or stimulation-related adverse events were encountered, with participants demonstrating a seven-point median improvement on the Upper-Extremity Fugl-Meyer Assessment. All individuals who enrolled with partial preservation of distal motor function exceeded minimal clinically important difference regardless of time since stroke, with a median improvement of 15 Upper-Extremity Fugl-Meyer Assessment points. These robust functional gains were directly correlated with cortical reorganization evidenced by increased ipsilesional metabolism. Our findings support the safety and feasibility of deep brain stimulation to the cerebellar dentate nucleus as a promising tool for modulation of late-stage neuroplasticity for functional recovery and the need for larger clinical trials. ClinicalTrials.gov registration: NCT02835443 .
MeSH term(s)	Humans ; Deep Brain Stimulation/adverse effects ; Treatment Outcome ; Stroke/therapy ; Stroke Rehabilitation ; Cerebellum ; Recovery of Function
Language	English
Publishing date	2023-08-14
Publishing country	United States
Document type	Clinical Trial, Phase I ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-023-02507-0
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Article ; Online: Schwann cell nodal membrane disruption triggers bystander axonal degeneration in a Guillain-Barré syndrome mouse model

Rhona McGonigal / Clare I. Campbell / Jennifer A. Barrie / Denggao Yao / Madeleine E. Cunningham / Colin L. Crawford / Simon Rinaldi / Edward G. Rowan / Hugh J. Willison

The Journal of Clinical Investigation, Vol 132, Iss

2022 Volume 14

Abstract: In Guillain-Barré syndrome (GBS), both axonal and demyelinating variants can be mediated by complement-fixing anti–GM1 ganglioside autoantibodies that target peripheral nerve axonal and Schwann cell (SC) membranes, respectively. Critically, the extent of ...

Abstract	In Guillain-Barré syndrome (GBS), both axonal and demyelinating variants can be mediated by complement-fixing anti–GM1 ganglioside autoantibodies that target peripheral nerve axonal and Schwann cell (SC) membranes, respectively. Critically, the extent of axonal degeneration in both variants dictates long-term outcome. The differing pathomechanisms underlying direct axonal injury and the secondary bystander axonal degeneration following SC injury are unresolved. To investigate this, we generated glycosyltransferase-disrupted transgenic mice that express GM1 ganglioside either exclusively in neurons [GalNAcT–/–-Tg(neuronal)] or glia [GalNAcT–/–-Tg(glial)], thereby allowing anti-GM1 antibodies to solely target GM1 in either axonal or SC membranes, respectively. Myelinated-axon integrity in distal motor nerves was studied in transgenic mice exposed to anti-GM1 antibody and complement in ex vivo and in vivo injury paradigms. Axonal targeting induced catastrophic acute axonal disruption, as expected. When mice with GM1 in SC membranes were targeted, acute disruption of perisynaptic glia and SC membranes at nodes of Ranvier (NoRs) occurred. Following glial injury, axonal disruption at NoRs also developed subacutely, progressing to secondary axonal degeneration. These models differentiate the distinctly different axonopathic pathways under axonal and glial membrane targeting conditions, and provide insights into primary and secondary axonal injury, currently a major unsolved area in GBS research.
Keywords	Autoimmunity ; Neuroscience ; Medicine ; R
Subject code	572
Language	English
Publishing date	2022-07-01T00:00:00Z
Publisher	American Society for Clinical Investigation
Document type	Article ; Online
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