Characterization of the neurological diseases associated with Mycoplasma pneumoniae infection and anti-glycolipid antibodies

Abstract

Mycoplasma pneumoniae infection often causes various neurological complications of both the central nervous system (CNS) and the peripheral nervous system. We retrospectively investigated the IgM and IgG antibodies to nine glycolipids [GM1, GM2, GM3, GD1a, GD1b, GD3, GT1b, GQ1b, and Gal-C (galactocerebroside)] and clinical features in neurological diseases associated with M. pneumoniae infection diagnosed in multiple hospitals throughout Japan between September 2010 and March 2012. Of the 46 patients with neurological diseases associated with M. pneumoniae infection, 27 were diagnosed with Guillain-Barré syndrome (GBS), 2 with Fisher syndrome (FS), 16 with CNS diseases, and 1 with both GBS and CNS disease. Anti-Gal-C IgM and IgG antibodies were most frequently detected (23/46, 50%). Patients with CNS diseases were younger than patients with GBS or FS, and IgM antibodies to Gal-C were more frequently detected in the patients with CNS diseases (41%) than in those with GBS or FS (13%). Of the nine patients who were positive for anti-Gal-C IgM antibody but lacked IgG antibody, we found the class-switch of anti-Gal-C antibody from IgM to IgG in two patients. The IgG antibodies appeared during their recovery phase, and the IgG belonged to the IgG1 subclass. Anti-Gal-C antibodies are closely associated with neurological diseases after M. pneumoniae infection. Particularly, anti-Gal-C IgM antibody is more frequently detected in younger patients affected with CNS involvement. The class-switch from IgM to IgG sometimes occurs in anti-Gal-C antibodies.

Experimental approach in research of Guillain–Barré syndrome: A range of pathogeneses mediated by molecular mimicry

“…This suggests the crucial role of aberrant class switch of anti‐GalC antibody‐specific B cells from IgM to IgG in the development of GBS after M. pneumoniae infection. Anti‐GalC IgG antibodies in GBS after M. pneumoniae infection belong to the IgG1 subclass, suggesting that IgG antibody response against GalC is caused through a T‐cell‐dependent process …”

Mechanism and spectrum of anti‐glycolipid antibody‐mediated chronic inflammatory demyelinating polyneuropathy

“…It was the first animal model of neuropathy induced by individual glycolipid . Often, antibodies to Gal‐C localized at both peripheral nervous system (PNS) and central nervous system (CNS) myelin are detected in GBS or CNS diseases after M. pneumoniae infection . Several studies have shown that M. pneumoniae comprises a component that mimics the carbohydrate structure of Gal‐C .…”

“…Several studies have shown that M. pneumoniae comprises a component that mimics the carbohydrate structure of Gal‐C . Based on electrophysiological studies, GBS cases with anti‐Gal‐C antibody are mostly classified as AIDP …”

“…42 Often, antibodies to Gal-C localized at both peripheral nervous system (PNS) and central nervous system (CNS) myelin are detected in GBS or CNS diseases after M. pneumoniae infection. [43][44][45] Several studies have shown that M. pneumoniae comprises a component that mimics the carbohydrate structure of Gal-C. 46,47 Based on electrophysiological studies, GBS cases with anti-Gal-C antibody are mostly classified as AIDP. 44,45 In GBS, the subclass of anti-glycolipid IgG antibody is predominantly IgG1 or IgG3, which activates the complement.…”

“…[43][44][45] Several studies have shown that M. pneumoniae comprises a component that mimics the carbohydrate structure of Gal-C. 46,47 Based on electrophysiological studies, GBS cases with anti-Gal-C antibody are mostly classified as AIDP. 44,45 In GBS, the subclass of anti-glycolipid IgG antibody is predominantly IgG1 or IgG3, which activates the complement. 48,49 Several previous studies have shown the deposition of C3d or membrane attack complex consisting of C5b-C9, indicating complement activation on the nerves of patients with GBS.…”