The reason for this is the similarity between structures on the surface of the bacteria and the body's own nerve-sheath structures (molecular mimicry). This leads to an immune reaction, which attacks both the mycoplasma and the surrounding myelin sheath of nerve pathways. "Antibodies recognize a certain glycolipid structure present at the cell membrane of the bacteria. These antibodies cross-react with and bind to galactocerebroside (GalC), one of the most common components of human myelin", explains Patrick Meyer Sauteur, the study's first author. This fatty substance ensures electrical conductivity of the nerve fibers. If it is destroyed, the patient experiences GBS, characterized by paralysis in arms and legs, weakness, and sensory disturbances.
https://goo.gl/G1suaU
Guillain-Barré syndrome (GBS) is an acute life-threatening disease of the nervous system that leads to sensory disturbances and acute flaccid paralysis. A group of researchers involving the University of Zurich has now shown for the first time that 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.
The bacterium Mycoplasma pneumoniae has been under suspicion for quite a while. Now, researchers at the University of Zurich, the University Children's Hospital Zurich, and the Erasmus University in Rotterdam have proved without a doubt that it is the culprit. In fact, mycoplasma is not only responsible for respiratory tract infections such as pneumonia in children and adults, it can also trigger Guillain-Barré syndrome (GBS) in infected individuals. The scientists have succeeded for the first time in culturing mycoplasma from a GBS patient in a laboratory setting.
Antibodies attack not only the bacteria but also the nerve pathways