Takahiro Furukawa1, Naoko Matsui2, Koji Fujita2, Ai Miyashiro2, Hiroyuki Nodera2, Yuishin Izumi2, Fumitaka Shimizu3, Katsuichi Miyamoto4, Yukitoshi Takahashi5, Takashi Kanda3, Susumu Kusunoki4, Ryuji Kaji2. 1. Department of Clinical Neuroscience, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, 770-8503, Japan. Electronic address: ft1981tf@gmail.com. 2. Department of Clinical Neuroscience, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, 770-8503, Japan. 3. Department of Neurology and Clinical Neuroscience, Yamaguchi University Graduate School of Medicine, Ube, 755-8505, Japan. 4. Department of Neurology, Kinki University School of Medicine, Osaka, 589-8511, Japan. 5. National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Shizuoka, 420-8688, Japan.
Abstract
BACKGROUND: Multifocal motor neuropathy (MMN) is characterized by clinical improvement with intravenous immunoglobulin and the frequent detection of anti-ganglioside antibodies. However, the immunological background of the neuronal damage in MMN is still unclear. OBJECTIVE: The aim of this study is to investigate abnormalities in the cytokine and chemokine profiles of MMN patients. METHODS: Sera from 16 patients with MMN, 16 patients with sporadic amyotrophic lateral sclerosis (ALS), and 15 patients with other non-inflammatory neurological diseases (ONDs) were analyzed for 27 cytokines and chemokines using a multiplex bead array. We also checked whether the altered cytokine/chemokine profile in the MMN group differed significantly in the presence or absence of abnormal electrophysiological findings. RESULTS: Serum IL-1Ra, IL-2, G-CSF, TNF-α, and TNFR1 levels were significantly higher in the MMN group than in the ONDs group. Of these, G-CSF and TNF-α also showed significant increases compared to the ALS group. Serum G-CSF and TNF-α levels were significantly higher in MMN patients presenting with focal demyelination including conduction block than in patients without any focal demyelination. CONCLUSIONS: Proinflammatory cytokines may contribute to peripheral nerve demyelination in MMN.
BACKGROUND:Multifocal motor neuropathy (MMN) is characterized by clinical improvement with intravenous immunoglobulin and the frequent detection of anti-ganglioside antibodies. However, the immunological background of the neuronal damage in MMN is still unclear. OBJECTIVE: The aim of this study is to investigate abnormalities in the cytokine and chemokine profiles of MMN patients. METHODS: Sera from 16 patients with MMN, 16 patients with sporadic amyotrophic lateral sclerosis (ALS), and 15 patients with other non-inflammatory neurological diseases (ONDs) were analyzed for 27 cytokines and chemokines using a multiplex bead array. We also checked whether the altered cytokine/chemokine profile in the MMN group differed significantly in the presence or absence of abnormal electrophysiological findings. RESULTS: Serum IL-1Ra, IL-2, G-CSF, TNF-α, and TNFR1 levels were significantly higher in the MMN group than in the ONDs group. Of these, G-CSF and TNF-α also showed significant increases compared to the ALS group. Serum G-CSF and TNF-α levels were significantly higher in MMN patients presenting with focal demyelination including conduction block than in patients without any focal demyelination. CONCLUSIONS: Proinflammatory cytokines may contribute to peripheral nerve demyelination in MMN.
Authors: Jared Ehrhart; Adam J Smith; Nicole Kuzmin-Nichols; Theresa A Zesiewicz; Israt Jahan; R Douglas Shytle; Seol-Hee Kim; Cyndy D Sanberg; Tuan H Vu; Clifton L Gooch; Paul R Sanberg; Svitlana Garbuzova-Davis Journal: J Neuroinflammation Date: 2015-06-28 Impact factor: 8.322