Mouse diaphragm assay for detection of antibodies against botulinum toxin type B.
Identifieur interne : 001363 ( Ncbi/Merge ); précédent : 001362; suivant : 001364Mouse diaphragm assay for detection of antibodies against botulinum toxin type B.
Auteurs : Dirk Dressler [Allemagne] ; M. Lange ; Hans BigalkeSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- Animals, Anti-Dyskinesia Agents (immunology), Anti-Dyskinesia Agents (therapeutic use), Antibodies (analysis), Biological Assay (methods), Botulinum Toxins (immunology), Botulinum Toxins (therapeutic use), Diaphragm (drug effects), Diaphragm (immunology), Dose-Response Relationship, Drug, Drug Interactions, Female, Humans, Male, Mice, Middle Aged, Time Factors, Torticollis (blood), Torticollis (drug therapy), Torticollis (immunology), Treatment Failure.
- MESH :
- chemical , analysis : Antibodies.
- chemical , immunology : Anti-Dyskinesia Agents, Botulinum Toxins.
- chemical , therapeutic use : Anti-Dyskinesia Agents, Botulinum Toxins.
- blood : Torticollis.
- drug effects : Diaphragm.
- drug therapy : Torticollis.
- immunology : Diaphragm, Torticollis.
- methods : Biological Assay.
- Animals, Dose-Response Relationship, Drug, Drug Interactions, Female, Humans, Male, Mice, Middle Aged, Time Factors, Treatment Failure.
Abstract
With the advent of a commercial preparation of botulinum toxin type B (BT-B) for treatment of cervical dystonia detection of antibodies against BT-B (BT-B-AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT-B 3 ng/ml the time to half-maximal twitch force reduction (paralysis time [PT]) was 69 +/- 4 min (n = 25). Addition of sera from patients with antibodies against BT-A produced a PT of 68 +/- 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 +/- 6 min (n = 30). When defined amounts of BT-B-AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT-B-AB added, thus producing a calibration curve. The threshold for BT-B-AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 +/- 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 +/- 2.9) and complete secondary failure of BT-B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 +/- 2,601 MU/injection series, 1.86 +/- 0.69 injection series before complete secondary therapy failure; 100.4 +/- 15.8 days between injection series with normal therapeutic effect) were tested, BT-B-AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT-B-AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT-B-AB titers in partial BT-B therapy failure.
DOI: 10.1002/mds.20625
PubMed: 16078216
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pubmed:16078216Le document en format XML
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<author><name sortKey="Dressler, Dirk" sort="Dressler, Dirk" uniqKey="Dressler D" first="Dirk" last="Dressler">Dirk Dressler</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Rostock University, Rostock, Germany. dirk.dressler@med.uni-rostock.de</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, Rostock University, Rostock</wicri:regionArea>
<wicri:noRegion>Rostock</wicri:noRegion>
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<author><name sortKey="Lange, M" sort="Lange, M" uniqKey="Lange M" first="M" last="Lange">M. Lange</name>
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<author><name sortKey="Bigalke, Hans" sort="Bigalke, Hans" uniqKey="Bigalke H" first="Hans" last="Bigalke">Hans Bigalke</name>
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<author><name sortKey="Dressler, Dirk" sort="Dressler, Dirk" uniqKey="Dressler D" first="Dirk" last="Dressler">Dirk Dressler</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Rostock University, Rostock, Germany. dirk.dressler@med.uni-rostock.de</nlm:affiliation>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Anti-Dyskinesia Agents (immunology)</term>
<term>Anti-Dyskinesia Agents (therapeutic use)</term>
<term>Antibodies (analysis)</term>
<term>Biological Assay (methods)</term>
<term>Botulinum Toxins (immunology)</term>
<term>Botulinum Toxins (therapeutic use)</term>
<term>Diaphragm (drug effects)</term>
<term>Diaphragm (immunology)</term>
<term>Dose-Response Relationship, Drug</term>
<term>Drug Interactions</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Middle Aged</term>
<term>Time Factors</term>
<term>Torticollis (blood)</term>
<term>Torticollis (drug therapy)</term>
<term>Torticollis (immunology)</term>
<term>Treatment Failure</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Antibodies</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Anti-Dyskinesia Agents</term>
<term>Botulinum Toxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Dyskinesia Agents</term>
<term>Botulinum Toxins</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Torticollis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Diaphragm</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Torticollis</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Diaphragm</term>
<term>Torticollis</term>
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<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Biological Assay</term>
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<term>Dose-Response Relationship, Drug</term>
<term>Drug Interactions</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Middle Aged</term>
<term>Time Factors</term>
<term>Treatment Failure</term>
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<front><div type="abstract" xml:lang="en">With the advent of a commercial preparation of botulinum toxin type B (BT-B) for treatment of cervical dystonia detection of antibodies against BT-B (BT-B-AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT-B 3 ng/ml the time to half-maximal twitch force reduction (paralysis time [PT]) was 69 +/- 4 min (n = 25). Addition of sera from patients with antibodies against BT-A produced a PT of 68 +/- 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 +/- 6 min (n = 30). When defined amounts of BT-B-AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT-B-AB added, thus producing a calibration curve. The threshold for BT-B-AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 +/- 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 +/- 2.9) and complete secondary failure of BT-B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 +/- 2,601 MU/injection series, 1.86 +/- 0.69 injection series before complete secondary therapy failure; 100.4 +/- 15.8 days between injection series with normal therapeutic effect) were tested, BT-B-AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT-B-AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT-B-AB titers in partial BT-B therapy failure.</div>
</front>
</TEI>
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<Title>Movement disorders : official journal of the Movement Disorder Society</Title>
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<ArticleTitle>Mouse diaphragm assay for detection of antibodies against botulinum toxin type B.</ArticleTitle>
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<Abstract><AbstractText>With the advent of a commercial preparation of botulinum toxin type B (BT-B) for treatment of cervical dystonia detection of antibodies against BT-B (BT-B-AB) becomes necessary. For this purpose, we carried out a mouse diaphragm assay (MDA) by continuous measurement of the twitch force of a mouse hemidiaphragm preparation elicited by electric stimulation of its phrenic nerve. After exposing the preparation to BT-B 3 ng/ml the time to half-maximal twitch force reduction (paralysis time [PT]) was 69 +/- 4 min (n = 25). Addition of sera from patients with antibodies against BT-A produced a PT of 68 +/- 5 min (n = 24), whereas addition of sera from controls with antibodies against tetanus toxoid produced a PT of 67 +/- 6 min (n = 30). When defined amounts of BT-B-AB were added to the MDA, PT was prolonged. This prolongation was correlated closely to the amount of BT-B-AB added, thus producing a calibration curve. The threshold for BT-B-AB detection was 0.4 mU/ml. When sera from 7 patients (4 women, 3 men; age 50.6 +/- 14.2 years) with cervical dystonia (Toronto Western Spasmodic Torticollis Rating Scale score, 18.9 +/- 2.9) and complete secondary failure of BT-B therapy (NeuroBloc; Elan Pharmaceuticals, Shannon, Ireland; 12,229 +/- 2,601 MU/injection series, 1.86 +/- 0.69 injection series before complete secondary therapy failure; 100.4 +/- 15.8 days between injection series with normal therapeutic effect) were tested, BT-B-AB titers of more than 10 mU/ml were found in all of them. The MDA can be used to measure neutralizing BT-B-AB titers quantitatively and with adequate sensitivity and specificity. Further studies are necessary to understand the role of intermediate BT-B-AB titers in partial BT-B therapy failure.</AbstractText>
</Abstract>
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