Anti-GM2 ganglioside antibodies are a biomarker for acute canine polyradiculoneuritis

Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain‐Barré syndrome (GBS); an aetiological relationship, however, remains to be demonstrated. In GBS, anti‐glycolipid antibodies (Abs) are considered as important disease medi...

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Published inJournal of the peripheral nervous system Vol. 18; no. 1; pp. 75 - 88
Main Authors Rupp, Angie, Galban-Horcajo, Francesc, Bianchi, Ezio, Dondi, Maurizio, Penderis, Jacques, Cappell, Joanna, Burgess, Karl, Matiasek, Kaspar, McGonigal, Rhona, Willison, Hugh J.
Format Journal Article
LanguageEnglish
Published Malden, USA Wiley Periodicals, Inc 01.03.2013
Wiley Subscription Services, Inc
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ISSN1085-9489
1529-8027
1529-8027
DOI10.1111/jns5.12011

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Abstract Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain‐Barré syndrome (GBS); an aetiological relationship, however, remains to be demonstrated. In GBS, anti‐glycolipid antibodies (Abs) are considered as important disease mediators. To address the possibility of common Ab biomarkers, the sera of 25 ACP dogs, 19 non‐neurological, and 15 epileptic control dogs were screened for IgG Abs to 10 glycolipids and their 1 : 1 heteromeric complexes using combinatorial glycoarrays. Anti‐GM2 ganglioside Abs were detected in 14/25 ACP dogs, and anti‐GA1 Abs in one further dog. All controls except for one were negative for anti‐glycolipid Abs. In this cohort of cases and controls, the glycoarray screen reached a diagnostic sensitivity of 60% and a specificity of 97%; a lower sensitivity (32%) was reported using a conventional glycolipid ELISA. To address the possible pathogenic role for anti‐GM2 Abs in ACP, we identified GM2 in canine sciatic nerve by both mass spectrometry and thin layer chromatography overlay. In immunohistological studies, GM2 was localized predominantly to the abaxonal Schwann cell membrane. The presence of anti‐GM2 Abs in ACP suggests that it may share a similar pathophysiology with GBS, for which it could thus be considered a naturally occurring animal model.
AbstractList Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain‐Barré syndrome (GBS); an aetiological relationship, however, remains to be demonstrated. In GBS, anti‐glycolipid antibodies (Abs) are considered as important disease mediators. To address the possibility of common Ab biomarkers, the sera of 25 ACP dogs, 19 non‐neurological, and 15 epileptic control dogs were screened for IgG Abs to 10 glycolipids and their 1 : 1 heteromeric complexes using combinatorial glycoarrays. Anti‐GM2 ganglioside Abs were detected in 14/25 ACP dogs, and anti‐GA1 Abs in one further dog. All controls except for one were negative for anti‐glycolipid Abs. In this cohort of cases and controls, the glycoarray screen reached a diagnostic sensitivity of 60% and a specificity of 97%; a lower sensitivity (32%) was reported using a conventional glycolipid ELISA. To address the possible pathogenic role for anti‐GM2 Abs in ACP, we identified GM2 in canine sciatic nerve by both mass spectrometry and thin layer chromatography overlay. In immunohistological studies, GM2 was localized predominantly to the abaxonal Schwann cell membrane. The presence of anti‐GM2 Abs in ACP suggests that it may share a similar pathophysiology with GBS, for which it could thus be considered a naturally occurring animal model.
Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain-Barré syndrome (GBS); an aetiological relationship, however, remains to be demonstrated. In GBS, anti-glycolipid antibodies (Abs) are considered as important disease mediators. To address the possibility of common Ab biomarkers, the sera of 25 ACP dogs, 19 non-neurological, and 15 epileptic control dogs were screened for IgG Abs to 10 glycolipids and their 1 : 1 heteromeric complexes using combinatorial glycoarrays. Anti-GM2 ganglioside Abs were detected in 14/25 ACP dogs, and anti-GA1 Abs in one further dog. All controls except for one were negative for anti-glycolipid Abs. In this cohort of cases and controls, the glycoarray screen reached a diagnostic sensitivity of 60% and a specificity of 97%; a lower sensitivity (32%) was reported using a conventional glycolipid ELISA. To address the possible pathogenic role for anti-GM2 Abs in ACP, we identified GM2 in canine sciatic nerve by both mass spectrometry and thin layer chromatography overlay. In immunohistological studies, GM2 was localized predominantly to the abaxonal Schwann cell membrane. The presence of anti-GM2 Abs in ACP suggests that it may share a similar pathophysiology with GBS, for which it could thus be considered a naturally occurring animal model.Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain-Barré syndrome (GBS); an aetiological relationship, however, remains to be demonstrated. In GBS, anti-glycolipid antibodies (Abs) are considered as important disease mediators. To address the possibility of common Ab biomarkers, the sera of 25 ACP dogs, 19 non-neurological, and 15 epileptic control dogs were screened for IgG Abs to 10 glycolipids and their 1 : 1 heteromeric complexes using combinatorial glycoarrays. Anti-GM2 ganglioside Abs were detected in 14/25 ACP dogs, and anti-GA1 Abs in one further dog. All controls except for one were negative for anti-glycolipid Abs. In this cohort of cases and controls, the glycoarray screen reached a diagnostic sensitivity of 60% and a specificity of 97%; a lower sensitivity (32%) was reported using a conventional glycolipid ELISA. To address the possible pathogenic role for anti-GM2 Abs in ACP, we identified GM2 in canine sciatic nerve by both mass spectrometry and thin layer chromatography overlay. In immunohistological studies, GM2 was localized predominantly to the abaxonal Schwann cell membrane. The presence of anti-GM2 Abs in ACP suggests that it may share a similar pathophysiology with GBS, for which it could thus be considered a naturally occurring animal model.
Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain-Barré syndrome (GBS); an aetiological relationship, however, remains to be demonstrated. In GBS, anti-glycolipid antibodies (Abs) are considered as important disease mediators. To address the possibility of common Ab biomarkers, the sera of 25 ACP dogs, 19 non-neurological, and 15 epileptic control dogs were screened for IgG Abs to 10 glycolipids and their 1:1 heteromeric complexes using combinatorial glycoarrays. Anti-GM2 ganglioside Abs were detected in 14/25 ACP dogs, and anti-GA1 Abs in one further dog. All controls except for one were negative for anti-glycolipid Abs. In this cohort of cases and controls, the glycoarray screen reached a diagnostic sensitivity of 60% and a specificity of 97%; a lower sensitivity (32%) was reported using a conventional glycolipid ELISA. To address the possible pathogenic role for anti-GM2 Abs in ACP, we identified GM2 in canine sciatic nerve by both mass spectrometry and thin layer chromatography overlay. In immunohistological studies, GM2 was localized predominantly to the abaxonal Schwann cell membrane. The presence of anti-GM2 Abs in ACP suggests that it may share a similar pathophysiology with GBS, for which it could thus be considered a naturally occurring animal model. [PUBLICATION ABSTRACT]
Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain-Barre syndrome (GBS); an aetiological relationship, however, remains to be demonstrated. In GBS, anti-glycolipid antibodies (Abs) are considered as important disease mediators. To address the possibility of common Ab biomarkers, the sera of 25 ACP dogs, 19 non-neurological, and 15 epileptic control dogs were screened for IgG Abs to 10 glycolipids and their 1 : 1 heteromeric complexes using combinatorial glycoarrays. Anti-GM2 ganglioside Abs were detected in 14/25 ACP dogs, and anti-GA1 Abs in one further dog. All controls except for one were negative for anti-glycolipid Abs. In this cohort of cases and controls, the glycoarray screen reached a diagnostic sensitivity of 60% and a specificity of 97%; a lower sensitivity (32%) was reported using a conventional glycolipid ELISA. To address the possible pathogenic role for anti-GM2 Abs in ACP, we identified GM2 in canine sciatic nerve by both mass spectrometry and thin layer chromatography overlay. In immunohistological studies, GM2 was localized predominantly to the abaxonal Schwann cell membrane. The presence of anti-GM2 Abs in ACP suggests that it may share a similar pathophysiology with GBS, for which it could thus be considered a naturally occurring animal model.
Acute canine polyradiculoneuritis ( ACP ) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain‐Barré syndrome ( GBS ); an aetiological relationship, however, remains to be demonstrated. In GBS , anti‐glycolipid antibodies (Abs) are considered as important disease mediators. To address the possibility of common Ab biomarkers, the sera of 25 ACP dogs, 19 non‐neurological, and 15 epileptic control dogs were screened for IgG Abs to 10 glycolipids and their 1 : 1 heteromeric complexes using combinatorial glycoarrays. Anti‐ GM2 ganglioside Abs were detected in 14/25 ACP dogs, and anti‐ GA1 Abs in one further dog. All controls except for one were negative for anti‐glycolipid Abs. In this cohort of cases and controls, the glycoarray screen reached a diagnostic sensitivity of 60% and a specificity of 97%; a lower sensitivity (32%) was reported using a conventional glycolipid ELISA . To address the possible pathogenic role for anti‐ GM2 Abs in ACP , we identified GM2 in canine sciatic nerve by both mass spectrometry and thin layer chromatography overlay. In immunohistological studies, GM2 was localized predominantly to the abaxonal Schwann cell membrane. The presence of anti‐ GM2 Abs in ACP suggests that it may share a similar pathophysiology with GBS , for which it could thus be considered a naturally occurring animal model.
Author Dondi, Maurizio
Penderis, Jacques
Cappell, Joanna
Rupp, Angie
McGonigal, Rhona
Galban-Horcajo, Francesc
Willison, Hugh J.
Burgess, Karl
Matiasek, Kaspar
Bianchi, Ezio
AuthorAffiliation 4 School of Veterinary Medicine, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK
1 Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK
3 Department of Veterinary Medical Sciences, University of Bologna, Bologna, Italy
2 Veterinary Teaching Hospital, University of Parma, Parma, Italy
5 Glasgow Polyomics, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK
6 Section of Clinical and Comparative Neuropathology, Department of Veterinary Clinical Sciences, Ludwig-Maximilians-University, Munich, Germany
AuthorAffiliation_xml – name: 2 Veterinary Teaching Hospital, University of Parma, Parma, Italy
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2013 Peripheral Nerve Society.
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Notes Lord Kelvin Adam Smith postgraduate scholarship scheme
ArticleID:JNS512011
Appendix S1. Materials and methods.
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1982; 56
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2010; 10
2002; 58
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2004; 127
1963; 86
2012; 242
2006; 74
1996; 39
2012; 366
1957; 226
2009; 80
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2007; 182
1997; 48
2013; 20
1988; 76
2008; 7
1982; 143
2000; 174
2002; 60
1988; 263
2010; 184
2011; 59
1998; 352
1997; 6
1995; 20
1997; 745
2010; 24
1971; 18
1986; 89
1993; 33
2011; 21
1969; 48
2011; 25
1972; 95
2009; 19
1998; 12
2009; 16
1981; 31
1996; 66
2001; 54
1990; 31
2001; 124
2004; 42
2006; 13
1981; 123
2002; 32
2009
1999; 66
2005; 80
2008; 204
2004
1999; 100
2011; 36
1992; 31
1991; 338
1999; 6
1972; 66
2003; 210
2009; 26
1965; 89
2012; 233
2005; 366
2000; 32
2002; 125
1967; 4
2006; 47
2010; 133
2005; 52
2005; 10
2002; 70
2012; 48
2001; 119
2001; 36
1998; 36
2005; 57
2005; 58
2001; 32
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Snippet Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain‐Barré syndrome (GBS); an...
Acute canine polyradiculoneuritis ( ACP ) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain‐Barré syndrome ( GBS ); an...
Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain-Barré syndrome (GBS); an...
Acute canine polyradiculoneuritis (ACP) is considered to be the canine equivalent of the human peripheral nerve disorder Guillain-Barre syndrome (GBS); an...
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StartPage 75
SubjectTerms Acute Disease
Animals
antibody
autoimmune neuropathy
Biomarkers - blood
Chromatography, Thin Layer
Diagnostic Imaging
dog
Dogs
Electric Stimulation
Electromyography
Enzyme-Linked Immunosorbent Assay
Evoked Potentials, Motor - physiology
Female
G(M2) Ganglioside - immunology
ganglioside
Guillain-Barré syndrome
Immunoglobulin G - blood
Magnetic Resonance Imaging
Male
Neurologic Examination
Polyradiculoneuropathy - blood
Polyradiculoneuropathy - diagnosis
Polyradiculoneuropathy - physiopathology
Polyradiculoneuropathy - veterinary
Sciatic Nerve - pathology
Spinal Cord - pathology
Statistics as Topic
Title Anti-GM2 ganglioside antibodies are a biomarker for acute canine polyradiculoneuritis
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Volume 18
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