Infectious and noninfectious triggers in Guillain–Barré syndrome. (July 2013)

• Record Type: Journal Article
• Authors: Wakerley, Benjamin R; Yuki, Nobuhiro
• Is Part Of: Expert review of clinical immunology. Volume 9:Number 7(2013)
• Page Start: 627
• Page End: 639
• Publication Date: 2013-07
• Subjects: acute inflammatory demyelinating polyneuropathy -- acute motor axonal neuropathy -- Bickerstaff brainstem encephalitis -- Campylobacter jejuni -- Fisher syndrome -- Guillain–Barré syndrome -- molecular mimicry; Clinical immunology -- Periodicals; 616.079
• DOI: 10.1586/1744666X.2013.811119
• Languages: English
• ISSNs: 1744-666X

Abstract

Guillain–Barré syndrome (GBS) is the commonest cause of acquired flaccid paralysis in the world and regarded by many as the prototype for postinfectious autoimmunity. Here the authors consider both infectious and noninfectious triggers of GBS and determine where possible what immunological mechanisms may account for this association. In approximately two-thirds of cases, an infectious trigger is reported in the weeks that lead up to disease onset, indicating that the host's response to infection must play an important role in disease pathogenesis. The most frequently identified bacteria, Campylobacter jejuni, through a process known as molecular mimicry, has been shown to induce cross-reactive anti-ganglioside antibodies, which can lead to the development of axonal-type GBS in some patients. Whether this paradigm can be extended to other infectious organisms or vaccines remains an important area of research and has public health implications. GBS has also been reported rarely in patients with underlying systemic diseases and immunocompromised states and although the exact mechanism is yet to be established, increased susceptibility to known infectious triggers should be considered most likely.