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 in | Journal of the peripheral nervous system Vol. 18; no. 1; pp. 75 - 88 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Malden, USA
Wiley Periodicals, Inc
01.03.2013
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
ISSN | 1085-9489 1529-8027 1529-8027 |
DOI | 10.1111/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. |
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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 – name: 3 Department of Veterinary Medical Sciences, University of Bologna, Bologna, Italy – name: 4 School of Veterinary Medicine, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK – name: 6 Section of Clinical and Comparative Neuropathology, Department of Veterinary Clinical Sciences, Ludwig-Maximilians-University, Munich, Germany – name: 1 Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK – name: 5 Glasgow Polyomics, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK |
Author_xml | – sequence: 1 givenname: Angie surname: Rupp fullname: Rupp, Angie organization: Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK – sequence: 2 givenname: Francesc surname: Galban-Horcajo fullname: Galban-Horcajo, Francesc organization: Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK – sequence: 3 givenname: Ezio surname: Bianchi fullname: Bianchi, Ezio organization: Veterinary Teaching Hospital, University of Parma, Parma, Italy – sequence: 4 givenname: Maurizio surname: Dondi fullname: Dondi, Maurizio organization: Veterinary Teaching Hospital, University of Parma, Parma, Italy – sequence: 5 givenname: Jacques surname: Penderis fullname: Penderis, Jacques organization: School of Veterinary Medicine – sequence: 6 givenname: Joanna surname: Cappell fullname: Cappell, Joanna organization: Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK – sequence: 7 givenname: Karl surname: Burgess fullname: Burgess, Karl organization: Glasgow Polyomics, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK – sequence: 8 givenname: Kaspar surname: Matiasek fullname: Matiasek, Kaspar organization: Section of Clinical and Comparative Neuropathology, Department of Veterinary Clinical Sciences, Ludwig-Maximilians-University, Munich, Germany – sequence: 9 givenname: Rhona surname: McGonigal fullname: McGonigal, Rhona organization: Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK – sequence: 10 givenname: Hugh J. surname: Willison fullname: Willison, Hugh J. email: Hugh.Willison@glasgow.ac.uk organization: Neuroimmunology Group, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23521648$$D View this record in MEDLINE/PubMed |
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Prevalence of C 1982; 56 1968; 7 2010; 10 2002; 58 1990; 54 2004; 127 1963; 86 2012; 242 2006; 74 1996; 39 2012; 366 1957; 226 2009; 80 2002; 196 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 e_1_2_7_5_1 e_1_2_7_3_1 e_1_2_7_7_1 e_1_2_7_19_1 Olby NJ (e_1_2_7_52_1) 2004 e_1_2_7_60_1 e_1_2_7_17_1 e_1_2_7_62_1 e_1_2_7_81_1 e_1_2_7_41_1 e_1_2_7_64_1 e_1_2_7_13_1 Lahunta A (e_1_2_7_18_1) 2009 e_1_2_7_43_1 e_1_2_7_66_1 e_1_2_7_11_1 e_1_2_7_45_1 e_1_2_7_68_1 e_1_2_7_47_1 e_1_2_7_26_1 e_1_2_7_49_1 e_1_2_7_28_1 Said G (e_1_2_7_61_1) 1981; 31 Vandevelde M (e_1_2_7_69_1) 1981; 123 Winer JB (e_1_2_7_80_1) 2001; 54 e_1_2_7_73_1 e_1_2_7_50_1 e_1_2_7_71_1 e_1_2_7_25_1 e_1_2_7_31_1 e_1_2_7_77_1 e_1_2_7_23_1 e_1_2_7_33_1 e_1_2_7_54_1 e_1_2_7_75_1 e_1_2_7_21_1 e_1_2_7_35_1 e_1_2_7_56_1 e_1_2_7_37_1 e_1_2_7_58_1 e_1_2_7_79_1 Cummings JF (e_1_2_7_15_1) 1972; 66 e_1_2_7_39_1 Staczek J (e_1_2_7_67_1) 1990; 54 Caudie C (e_1_2_7_9_1) 2002; 60 e_1_2_7_6_1 e_1_2_7_4_1 e_1_2_7_16_1 e_1_2_7_40_1 e_1_2_7_82_1 e_1_2_7_2_1 e_1_2_7_14_1 e_1_2_7_42_1 e_1_2_7_63_1 e_1_2_7_12_1 e_1_2_7_44_1 e_1_2_7_65_1 e_1_2_7_10_1 e_1_2_7_46_1 e_1_2_7_48_1 e_1_2_7_27_1 e_1_2_7_29_1 Bossi P (e_1_2_7_8_1) 1998; 36 Prasad KN (e_1_2_7_55_1) 2001; 32 e_1_2_7_72_1 e_1_2_7_51_1 e_1_2_7_70_1 e_1_2_7_30_1 e_1_2_7_53_1 e_1_2_7_76_1 e_1_2_7_24_1 e_1_2_7_32_1 e_1_2_7_74_1 e_1_2_7_22_1 e_1_2_7_34_1 e_1_2_7_57_1 e_1_2_7_20_1 e_1_2_7_36_1 e_1_2_7_59_1 e_1_2_7_78_1 e_1_2_7_38_1 |
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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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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 |
URI | https://api.istex.fr/ark:/67375/WNG-76FH3Z1R-0/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1111/jns5.12011 https://www.ncbi.nlm.nih.gov/pubmed/23521648 https://www.proquest.com/docview/1318875762 https://www.proquest.com/docview/1319619856 https://www.proquest.com/docview/1328520819 https://pubmed.ncbi.nlm.nih.gov/PMC4854321 |
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