What is the role of C jejuni antibodies in the etiology of Guillain-Barre syndrome (GBS)?

Updated: May 04, 2018
  • Author: Michael T Andary, MD, MS; Chief Editor: Milton J Klein, DO, MBA  more...
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Answer

The virulence of C jejuni is thought to result from the presence of specific antigens in its capsule that are shared with nerves. Immune responses directed against capsular lipopolysaccharides produce antibodies that cross-react with myelin to cause demyelination.

C jejuni infections also generate anti-ganglioside antibodies—including to the gangliosides GM1, GD1a, GalNac-GD1a, and GD1b—that are commonly found in patients with AMAN and AMSAN, the axonal subtypes of GBS. (Patients with C. jejuni enteritis not complicated by GBS, however, do not produce the specific anti-ganglioside antibodies.)

Even in the subgroup of patients with GM1 antibodies, however, the clinical manifestations vary. Host susceptibility is probably one determinant in the development of GBS after infectious illness. [25, 27]

Although GM1 antibodies can also be found in patients with demyelinating GBS, they are much less common in these cases. C. jejuni infection can also generate antibodies to the ganglioside GQ1b, a component of oculomotor nerve myelin; these are associated with MFS.


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