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Yukihiro Nishimoto

Publications and source records attributed to Yukihiro Nishimoto.

8 recordsLinked to original sources
PubMed2006

Leukocyte and complement activation by GM1-specific antibodies is associated with acute motor axonal neuropathy in rabbits.

Acute motor axonal neuropathy (AMAN) in humans is associated with the presence of GM1-specific antibodies. Immunization of rabbits with GM1-containing ganglioside mixtures, purified GM1, or Campylobacter jejuni lipo-oligosaccharide exhibiting a GM1-like structure elicits GM1-specific antibodies, but axonal polyneuropathy only occurs in a subset of animals. This study aimed to dissect the molecular basis for the variable induction of AMAN in rabbits. Therefore, we analyzed the pro-inflammatory characteristics of GM1-specific antibodies in plasma samples from ganglioside-immunized rabbits with and without neurological deficits. GM1-specific plasma samples from all rabbits with AMAN were capable of activating both complement and leukocytes, in contrast to none of the plasma samples from rabbits without paralysis. Furthermore, GM1-specific IgG-mediated activation of leukocytes was detected before the onset of clinical signs. These data suggest that AMAN only occurs in rabbits that develop GM1-specific antibodies with pro-inflammatory properties.

Acute Disease↗
PubMed2004

Various immunization protocols for an acute motor axonal neuropathy rabbit model compared.

Various ganglioside immunization protocols were examined to refine the procedure for establishing an animal model of acute motor axonal neuropathy. The most effective was subcutaneous injection of an emulsion of 2.5mg of bovine brain ganglioside mixtures, keyhole lympet hemocyanin, and complete Freund's adjuvant to Japanese white rabbits, repeated at 3-week intervals. Under that protocol, all the rabbits developed marked flaccid paralysis associated with plasma anti-GM1 IgG antibody. This acute motor axonal neuropathy rabbit model also could be reproduced by the use of incomplete Freund's adjuvant, methylated bovine serum albumin, and New Zealand white rabbits. These results provide useful information for the confirmation of and further research on the model.

Acute Disease↗
PubMed2004

Carbohydrate mimicry between human ganglioside GM1 and Campylobacter jejuni lipooligosaccharide causes Guillain-Barre syndrome.

Molecular mimicry between microbial and self-components is postulated as the mechanism that accounts for the antigen and tissue specificity of immune responses in postinfectious autoimmune diseases. Little direct evidence exists, and research in this area has focused principally on T cell-mediated, antipeptide responses, rather than on humoral responses to carbohydrate structures. Guillain-Barré syndrome, the most frequent cause of acute neuromuscular paralysis, occurs 1-2 wk after various infections, in particular, Campylobacter jejuni enteritis. Carbohydrate mimicry [Galbeta1-3GalNAcbeta1-4(NeuAcalpha2-3)Galbeta1-] between the bacterial lipooligosaccharide and human GM1 ganglioside is seen as having relevance to the pathogenesis of Guillain-Barré syndrome, and conclusive evidence is reported here. On sensitization with C. jejuni lipooligosaccharide, rabbits developed anti-GM1 IgG antibody and flaccid limb weakness. Paralyzed rabbits had pathological changes in their peripheral nerves identical with those present in Guillain-Barré syndrome. Immunization of mice with the lipooligosaccharide generated a mAb that reacted with GM1 and bound to human peripheral nerves. The mAb and anti-GM1 IgG from patients with Guillain-Barré syndrome did not induce paralysis but blocked muscle action potentials in a muscle-spinal cord coculture, indicating that anti-GM1 antibody can cause muscle weakness. These findings show that carbohydrate mimicry is an important cause of autoimmune neuropathy.

Animals↗
PubMed2004

[Outcome after Guillain-Barré syndrome: comparison of motor function status and changes in social life].

Effects on the motor function and social life of the patients after Guillain-Barré syndrome (GBS) were studied. A letter of inquiry was sent to the patients in November 2001; 98 patients responded validly. The questionnaire had questions with 3 possible answers related to situations at work, at home, and about leisure activities. The Hughes functional grade, which evaluates physical conditions, and arm disability scale scores were assessed. Although the assessments showed good recovery in most patients who had had a job, 31% had to quit work, and 17% had to discontinue their leisure activities. These physical assessments accurately reflected the severity of the conditions of the patients given in-home care (8%) because daily life activities depend on muscle strength. Of the 75 patients who had no, or minimal, neurological symptoms or signs in both assessments, 53% reported one or more changes in their social lives. We conclude that the questionnaire answers show that GBS patients may have serious psychosocial outcomes that are not measurable by the usual physical assessments. These findings may be a help when considering the rehabilitation of GBS patients and their return to social life.

Activities of Daily Living↗
PubMed2004

[Details about the first medical examinations of patients with Guillain-Barré or Fisher syndromes].

Randomized controlled trials have shown beneficial responses to plasma exchange and intravenous immunoglobulin in Guillain-Barré syndrome (GBS), but details about the first medical examination of patients with GBS and Fisher syndrome (FS) have not been reported. We investigated the period from first consultations to treatment after the onset of patients with GBS and FS. A questionnaire was used to collect informations on 247 patients with GBS and 125 with FS, all of whom had been referred to our neuroimmunological laboratory informations between January 2001 and October 2001 for serum anti-ganglioside antibody tests. A letter of inquiry was sent to the primary physicians; 150 (61%) patients with GBS and 72 (58%) with FS responded validly. Patients with GBS generally consulted an internist [58%, neurologist (21%)] or orthopedist (17%), those with FS an internist [52%, neurologist (26%)] or ophthalmologist (25%). Consultation with a neurologist usually came after one with a physician. We conclude that physicians should be aware that patients may have GBS or FS, and that such recognition is useful for early diagnosis and treatment of these syndromes.

Guillain-Barre Syndrome↗
PubMed2004

[Intravenous immunoglobulin therapy for Guillain-Barré syndrome in Japan: changes in treatment after its inclusion in health insurance coverage].

In December 2000, health insurance in Japan was instituted for the use of intravenous immunoglobulin (IVIg) therapy for the acute phase of Guillain-Barré syndrome (GBS) that required aid to walk or worse. A nation-wide questionnaire survey was made to investigate the changes in treatment. In September 2002, a letter of inquiry was sent to experienced physicians in 620 teaching hospitals associated with the Societas Neurologica Japonica and 417 associated with the Societas Paediatrica Japonica. Totally, 356 neurologists (57%) and 223 pediatricians (53%) responded. After the introduction of IVIg health insurance coverage, more than 90% thought that GBS patients should be hospitalized and given treatment. The frequency of hospitals with an intensive care unit, however, was 70%. Before IVIg therapy's inclusion in health insurance coverage, many neurologists selected plasmapheresis (88%) rather than IVIg (4%) therapy, whereas pediatricians preferred IVIg (49%) to plasmapheresis (12%). After its inclusion, 75% of neurologists selected IVIg rather than plasmapheresis (21%), whereas pediatricians selected IVIg (86%) over plasmapheresis (5%). In March 2003, new payment system based on Diagnosis Procedure Combination was introduced into 82 large hospitals, and leads to difficulties to select IVIg in the hospitals. The payment system should be revised.

Guillain-Barre Syndrome↗
PubMed2003

Acute motor axonal neuropathy rabbit model: immune attack on nerve root axons.

Macrophages in the periaxonal space and surrounding intact myelin sheath are the most prominent pathological feature of acute motor axonal neuropathy (AMAN). We describe this characteristic in nerve roots from paralyzed rabbits immunized with bovine brain ganglioside or GM1. IgG was deposited on nerve root axons. Distal nerve conduction was preserved, and late F wave components were absent during the acute phase. Initial lesions were located mainly on nerve root axons, as in human AMAN. This study thus provides supportive evidence that the rabbits constitute a model of AMAN.

Action Potentials↗