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Autoantibody-Mediated Dysfunction of Sympathetic Neurons in Guillain-Barré Syndrome
Helmar C. Lehmann, MD;
Parastoo Jangouk, MD;
Eva K. Kierysch, MD;
Gerd Meyer zu Hörste, MD;
Hans-Peter Hartung, MD;
Bernd C. Kieseier, MD
Arch Neurol. 2010;67(2):203-210.
Objective To investigate a pathologic immune response to autonomic nerve fibers in Guillain-Barré syndrome (GBS).
Design We compared the effects of purified IgG from patients with GBS, multiple sclerosis, and chronic inflammatory demyelinating polyneuropathy on transmitter synthesis and synaptic transmission in an in vitro model of sympathetic neurons and cardiomyocytes.
Subjects Three patients with GBS, 2 with chronic inflammatory demyelinating polyradiculoneuropathy, and 2 with relapsing-remitting multiple sclerosis.
Results Incubation of sympathetic neurons with GBS-IgG resulted in an upregulation of tyrosine hydroxylase and caused a relative increase of noradrenaline levels. In cocultures of sympathetic neurons and cardiomyocytes, GBS-IgG altered the synaptic transmission, as assessed by changes in the average cardiomyocyte beat rate. These effects could be neutralized by preincubation of sympathetic neurons with intravenous immunoglobulins.
Conclusion Our findings indicate that in GBS, circulating antibodies directed against sympathetic neurons may contribute to autonomic dysfunction via functionally relevant changes in the noradrenaline synthesis.
Author Affiliations: Department of Neurology (Drs Lehmann, Jangouk, Meyer zu Hörste, Hartung, and Kieseier), and Institute of Clinical Chemistry and Laboratory Diagnostics (Dr Kierysch), Heinrich-Heine University, Düsseldorf, Germany.
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