Giuseppe
Emeritus
Autoantibody-Mediated Dysfunction of Sympathetic Neurons in Guillain-Barre Syndrome (Arch Neurol., abstract, edited)
Autoantibody-Mediated Dysfunction of Sympathetic Neurons in Guillain-Barr? Syndrome
Helmar C. Lehmann, MD; Parastoo Jangouk, MD; Eva K. Kierysch, MD; Gerd Meyer zu H?rste, 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-Barr? 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 H?rste, Hartung, and Kieseier), and Institute of Clinical Chemistry and Laboratory Diagnostics (Dr Kierysch), Heinrich-Heine University, D?sseldorf, Germany.
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<cite cite="http://archneur.ama-assn.org/cgi/content/abstract/67/2/203?etoc">Arch Neurol -- Abstract: Autoantibody-Mediated Dysfunction of Sympathetic Neurons in Guillain-Barre Syndrome, February 2010, Lehmann et al. 67 (2): 203</cite>Helmar C. Lehmann, MD; Parastoo Jangouk, MD; Eva K. Kierysch, MD; Gerd Meyer zu H?rste, 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-Barr? 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 H?rste, Hartung, and Kieseier), and Institute of Clinical Chemistry and Laboratory Diagnostics (Dr Kierysch), Heinrich-Heine University, D?sseldorf, Germany.
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