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From the Department of Neurology (Drs. Koga, Yuki, and Hirata) and Institute for Medical Science (S. Koike), Dokkyo University School of Medicine, Tochigi, Department of Microbiology (Dr. Takahashi), Tokyo Metropolitan Institute of Public Health, and Department of Biochemistry II (Dr. Furukawa), Nagoya University School of Medicine, Aichi, Japan; and Institute for Biological Sciences (Drs. Gilbert and Li), National Research Council Canada, Ottawa, Ontario, Canada.
Address correspondence and reprint requests to Dr. M. Koga, Department of Neurology, Dokkyo University School of Medicine, Kitakobayashi 880, Mibu, Shimotsuga, Tochigi 321-0293, Japan; e-mail: kogamrk{at}dokkyomed.ac.jp
Objective: To assess the production mechanism of anti-GQ1b autoantibody in Fisher syndrome (FS).
Methods: The authors conducted a prospective case-control serologic study of five antecedent infections (Campylobacter jejuni, cytomegalovirus, Epstein–Barr virus, Mycoplasma pneumoniae, and Haemophilus influenzae) in 73 patients with FS and 73 sex- and age-matched hospital controls (HCs). Serologic evidence in FS patients of C. jejuni (21%) and H. influenzae (8%) infections was present significantly more often than in the HCs. None of the five pathogens examined was found in the 49 (67%) patients with FS. Anti-GQ1b IgG antibody was detected in most FS patients infected with C. jejuni or H. influenzae. Mass spectrometry analysis identified a C. jejuni strain (CF93-6) carrying a GT1a-like lipo-oligosaccharide (LOS) that had been isolated from an FS patient. Immunization of complex ganglioside-lacking knockout mice with the GT1a-like LOS generated IgG class monoclonal antibodies (mAbs) that reacted with GQ1b and GT1a. Thin-layer chromatography with immunostaining showed that anti-GQ1b mAb bound to the C. jejuni LOS (50% of the 20 FS-related strains) more commonly than in the Guillain–Barré syndrome (GBS)–related (7% of 70) or enteritis-related (20% of 65) strains. Anti-GM1 and anti-GD1a mAbs also reacted with the LOS from some FS-related strains (both 20%), but binding frequencies were higher in the GBS-related strains (74 and 57%). The GQ1b epitope was detected in 4 (40%) of the 10 FS-related H. influenzae strains but was absent in strains from patients with GBS (n = 4) and uncomplicated respiratory infections (n = 10).
Conclusions: C. jejuni and H. influenzae are related to Fisher syndrome (FS) development, and production of anti-GQ1b autoantibody is mediated by the GQ1b-mimicking lipo-oligosaccharides on those bacteria. The causative agents remain unclear in the majority of patients with FS.
Additional material related to this article can be found on the Neurology Web site. Go to www.neurology.org and scroll down the Table of Contents for the May 10 issue to find the title link for this article.
Supported in part by grants-in-aid from the Ichiro Kanehara Foundation, the Kanae Foundation for Life and Socio-Medical Science, and the Japan Intractable Diseases Research Foundation; by a grant for Scientific Research (B) (KAKENHI 14370210 to N.Y.) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan; a Research Grant for Neuroimmunological Diseases from the Ministry of Health, Labour, and Welfare of Japan; a Health Sciences Research Grant (Research on Psychiatric and Neurological Diseases and Mental Health) from the Ministry of Health, Labour, and Welfare of Japan; and a grant from the Human Frontier Science Program (RGP0038/2003-C).
Received October 26, 2004. Accepted January 12, 2005.
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