Respiratory Tract Bacterium Triggers Serious Nervous System Disease

Guillain-Barré syndrome (GBS) is an acute post infectious immune-mediated polyneuropathy and an acute life-threatening disease of the nervous system that leads to sensory disturbances and acute flaccid paralysis.

Although preceding respiratory tract infections with Mycoplasma pneumoniae have been reported in some cases, the role of M. pneumoniae in the pathogenesis of GBS remains unclear. Bacteria, which often cause pneumonia, can trigger the autoimmune disease GBS. Antibodies that not only attack the bacteria but also the outer layer of the body's own nerve cells are a critical step in the pathogenesis of GBS after this respiratory infection.

Scientists at the Erasmus University Medical Center (Rotterdam, The Netherlands) and their colleagues investigated a total of 189 adults and 24 children with GBS for the presence of antibodies to mycoplasma, as an indication of a recent bacterial infection, and galactocerebroside (GalC) as the suspected trigger for GBS, and compared them with 677 healthy individuals as controls.

Anti–M. pneumoniae immunoglobulin (Ig) M antibodies were detected in GBS patients and healthy controls in 3% and 0% of adults and 21% and 7% of children respectively. The anti-GalC antibodies immunoglobulins M and/or G (IgM and/or IgG) were found in 4% of adults and 25% of children with GBS. Anti-GalC-positive patients showed more frequent preceding respiratory symptoms, cranial nerve involvement, and a better outcome. Anti-GalC antibodies correlated with anti–M. pneumoniae antibodies and cross-reacted with different M. pneumoniae strains. Anti-GalC IgM antibodies were not only found in GBS patients with M. pneumoniae infection, but also in patients without neurological disease whereas anti-GalC IgG was exclusively found in patients with GBS.

Interestingly, the anti-GalC antibodies were also found in patients without GBS who had recently been infected with mycoplasma. However, these were all of the antibody isotype M (immunoglobulin M, IgM), the earliest antibody type elicited during an acute immune response. By contrast, the anti-GalC antibodies in the GBS patients were of the isotype IgG. Peter M. Meyer Sauteur, MD, the lead author of the study said, “We therefore assume that this class switch of the antibody isotype may contribute to the pathogenesis of GBS. In fact, this antibody isotype class switch is also assumed as a critical step in the development of other autoimmune diseases. Immunotherapies based on that premise may thus be a new possible treatment option for GBS.” The study was published on September 26, 2016, in the journal Annals of Neurology.

Related Links:
Erasmus University Medical Center