The common pneumonia-causing bacterium Mycoplasma pneumoniae can trigger Guillain-Barré syndrome, an autoimmune disease, because antibodies attacking the bacterium can mistake molecules on nerve cells for the intended target.
The study, “Mycoplasma pneumoniae triggering the Guillain-Barré syndrome: a case-control study,” published in the journal Annals of Neurology, gives researchers new insights into the molecular events that lead to the disease, and may one day be used to develop ways of preventing pneumonia from progressing to autoimmune conditions.
Researchers have long suspected that Guillain-Barré syndrome is somehow linked to airway or stomach infections, as it tends to appear shortly after an infection. The condition is characterized by muscle weakness that can rapidly progress and ultimately cause paralysis.
Scientists know that Guillain-Barré is caused by antibodies against a molecule called galactocerebroside (GalC), which is present in the myelin sheets covering nerve cells. When myelin gets destroyed by the immune system, neurons can no longer properly signal for muscles to move. Difficulty breathing and a lack of blood pressure control further complicates the condition.
For the first time, researchers at Erasmus University Medical Center, in the Netherlands, and at University Children’s Hospital Zurich, managed to isolate Mycoplasma pneumoniae from a patient with Guillain-Barré syndrome. To test if the condition was linked to the bacterial infection, the team also isolated antibodies against GalC.
As suspected, the GalC antibodies also reacted to the bacteria found in the patient. This can happen when two molecules are fairly similar, and the team showed that the GalC antibodies also reacted weakly to other types of Mycoplasma, but not to other types of bacteria.
These findings prompted the researchers to study the association in a larger group of people. They looked at 189 adults and 24 children with Guillain-Barré syndrome to examine if they had antibodies to Mycoplasma pneumoniae. The presence of such antibodies would indicate that a patient was recently infected. Researchers also looked for antibodies against GalC, and compared the data to 677 healthy controls.
Results showed that 3 percent of the adults, and 21 percent of the children had had a recent Mycoplasma infection. This percentage was much higher than in healthy controls, where no adults and 7 percent of children had Mycoplasma antibodies.
Antibodies against GalC were found in almost the same proportions: 3 percent in adults and 25 percent in children. Researchers also noted that anti-GalC antibodies were found in people who recently had a Mycoplasma infection, but had not developed Guillain-Barré syndrome.
This finding gave the team a clue as to what was going on. All of the GalC antibodies in patients without disease were of one type, called IgM. This type of antibodies is usually seen early on in an immune response. But among patients with Guillain-Barré syndrome, the antibodies were of a type called IgG.
“We therefore assume that this class switch of the antibody isotype may contribute to the pathogenesis of Guillain-Barré syndrome”, Patrick Meyer Sauteur, the study’s first author, said in a press release.
“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 Guillain-Barré syndrome,” he added.
