Triggers of Guillain–Barré Syndrome: Campylobacter jejuni Predominates

Abstract

Guillain–Barré syndrome (GBS) is a rare immune-mediated acute polyradiculo-neuropathy that typically develops after a previous gastrointestinal or respiratory infection. This narrative overview aims to summarise and discuss current knowledge and previous evidence regarding triggers and pathophysiology of GBS. A systematic search of the literature was carried out using suitable search terms. The most common subtypes of GBS are acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). The most common triggers of GBS, in three quarters of cases, are previous infections. The most common infectious agents that cause GBS include Campylobacter jejuni (C. jejuni), Mycoplasma pneumoniae, and cytomegalovirus. C. jejuni is responsible for about a third of GBS cases. GBS due to C. jejuni is usually more severe than that due to other causes. Clinical presentation of GBS is highly dependent on the structure of pathogenic lipo-oligosaccharides (LOS) that trigger the innate immune system via Toll-like-receptor (TLR)-4 signalling. AIDP is due to demyelination, whereas in AMAN, structures of the axolemma are affected in the nodal or inter-nodal space. In conclusion, GBS is a neuro-immunological disorder caused by autoantibodies against components of the myelin sheath or axolemma. Molecular mimicry between surface structures of pathogens and components of myelin or the axon is one scenario that may explain the pathophysiology of GBS.

Diagnostic Pitfalls in Guillain–Barré Syndrome: Case Report and Literature Review

“…The results of all of these measurements were negative for our patient. Mycoplasma pneumoniae infection, as well as Mycobacterium tuberculosis , Borrelia burgdorferi , Epstein–Barr virus, cytomegalovirus and Toxoplasma gondii infection [ 61 , 62 , 63 , 64 , 65 ], all known as trigger factors for GBS, could not be identified in our patient.…”

Non-neutralizing antibodies to SARS-Cov-2-related linear epitopes induce psychotic-like behavior in mice

“…Besides the respiratory system, if the antigen of SARS-CoV-2 is highly homologous with the nervous system tissue, then the cross-reactive antibody can also trigger the corresponding autoimmune response. For example, Epstein–Barr virus (EBV) infection has been linked to multiple sclerosis ( Lanz et al, 2022 ), and Campylobacter jejuni is responsible for about a third of Guillain-Barré cases ( Finsterer, 2022 ). According to the BLAST analysis ( Supplementary Table S2 ), S1-111 is homologous to the OCA2 protein, which is hypothesized to be an integral membrane protein involved in small molecule transport, specifically tyrosine ( Yang et al, 2019 ).…”

Molecular Targets in Campylobacter Infections

“…The severity of initial enteritis is significantly associated with the risk of post-infectious sequelae, which may appear weeks or months after the intestinal infection [ 15 ]. Post-infectious sequelae include Guillain–Barré-Syndrome (GBS) [ 16 , 17 ], reactive arthritis [ 18 ], inflammatory bowel diseases [ 19 , 20 , 21 ] or irritable bowel syndrome [ 18 ]. In rare cases, Campylobacter bacteremia occurring in immunocompromised individuals may lead to meningitis [ 22 ] or cardiovascular diseases [ 23 ] (for reviews concerning post-infectious complications, see [ 4 , 13 , 24 , 25 , 26 ]).…”