Anti-GM1 IgG antibodies and campylobacter bacteria in Guillain-Barré syndrome: Evidence of molecular mimicry

1995 ◽  
Vol 38 (2) ◽  
pp. 170-175 ◽  
Author(s):  
Peter G. Oomes ◽  
Bart C. Jacobs ◽  
Maarten P. H. Hazenberg ◽  
John R. J. Bänffer ◽  
Frans G. A. van der Meché
2018 ◽  
Vol 39 (7) ◽  
pp. 1291-1292 ◽  
Author(s):  
Sonia Quintas ◽  
Rocío López Ruiz ◽  
Carmen Ramos ◽  
José Vivancos ◽  
Gustavo Zapata-Wainberg

1995 ◽  
Vol 38 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Isabel Illa ◽  
Nicolau Ortiz ◽  
Eduard Gallard ◽  
Candido Juarez ◽  
Josep M. Grau ◽  
...  

2014 ◽  
Vol 2 (1) ◽  
pp. 28-35 ◽  
Author(s):  
Nurun Nahar Mawla ◽  
Shahin Sultana ◽  
Nayareen Akhter

Guillain-Barré syndrome (GBS), a neurologic disease that produces ascending paralysis, affects people all over the world. Acute infectious illness precedes 50%-75% of the GBS cases. Although many infectious agents have been associated with GBS, the strongest documented association is with Campylobacter infection. The first line of evidence supporting Campylobacter infection as a trigger of GBS is anecdotal reports. The second line of evidence is serological surveys, which have demonstrated that sera from GBS patients contain anti Campylobacter jejuni antibodies, consistent with recent infection. Finally, culture studies have proven that a high proportion of GBS patients have C. jejuni in their stools at the time of onset of neurological symptoms. One of every 1058 Campylobacter infections results in GBS. Sialic acid containing lipooligosaccharides (LOS) biosynthesis gene locus are associated with GBS and the expression of ganglioside mimicking structures. GM1a was the most prevalent ganglioside mimic in GBS associated strains. Molecular mimicry between C. jejuni LOS and gangliosides in human peripheral nerves, and cross-reactive serum antibody precipitate the majority of GBS cases in Bangladesh, like worldwide. DOI: http://dx.doi.org/10.3329/dmcj.v2i1.17794 Delta Med Col J. Jan 2014; 2(1): 28-35


Author(s):  
Rahmathulla S. Rahman ◽  
Moayyad S. Bauthman ◽  
Amer M. Alanazi ◽  
Naif N. Alsillah ◽  
Ziyad M. Alanazi ◽  
...  

Guillain–Barré syndrome (GBS) is a polyradiculoneuropathy autoimmune disease that is characterized by significant inflammation that affects the peripheral nervous system in a rapidly progressive pattern that is mainly clinically presented by muscle weakness. The present literature review aims to broadly discuss GBS: etiology, pathophysiology and management in order to gain an understading of the existing studies that are relevant to this literature review. Among the reported antibodies, anti-GM1 and anti-GQ1B have been reported to be responsible for attacking and damaging either the neuromuscular junctions or peripheral nerves. Moreover, it has been found that the anti-GD1a antibodies in patients bind to the neuromuscular junction and also bind to the nodes of Ranvier of the peripheral nerves and the paranodal myelin of the affected nerves. Reports have shown that this disease is identified as special forms of neuropathies that develop in immune-mediated, post-infection sequelae. Furthermore, in another study it was reported that Molecular mimicry has been previously reported to significantly correlate with the development of the disease as it was investigated in animal models. In addition, Campylobacter jejuni, a pathogen that causes gastrointestinal infections has been previously reported to predispose to the development of GBS in humans. However, scientists have found that plasma exchange and intravenous immunoglobulins (IVIG) remain the most significant and efficacious factors in managing the disease. Nevertheless, recent trials have investigated other approaches that are less efficacious and can lead to serious adverse events and complications. 


2021 ◽  
pp. 1-3
Author(s):  
Rachel Koreen ◽  
◽  
Jacob Chevlen DO ◽  

Guillain Barre Syndrome (GBS) is a rare neurologic disorder in which the immune system mistakenly attacks the peripheral nervous system due to molecular mimicry. GBS symptoms can range from a mild episode of weakness to devastating paralysis and respiratory failure. The exact cause of GBS is unknown, but it is often thought to be due to a preceding viral infection or rarely due to vaccination. To date, there has only been one reported case of Guillain Barre Syndrome associated with the administration of Ad26.COV2.S vaccine (Janssen/Johnson & Johnson COVID-19 vaccine) [3]. Here, we describe the case of a 59-year-old woman who received the Johnson & Johnson COVID-19 vaccine and subsequently developed symptoms consistent with GBS. Unfortunately, due to failure to obtain lumbar puncture (LP) and electromyography (EMG), it is only possible to diagnose Guillain Barre syndrome with Level 3 diagnostic certainty using the Brighton criteria [6]. We are of the opinion that our patient developed GBS subsequent to the vaccination, but not necessarily consequent to the vaccination, as it remains possible that she may have contracted an asymptomatic infection prior to inoculation


2006 ◽  
Vol 35 (4) ◽  
pp. 277-279 ◽  
Author(s):  
Joachim Schessl ◽  
Kei Funakoshi ◽  
Keiichiro Susuki ◽  
Ralf Gold ◽  
Rudolf Korinthenberg

2004 ◽  
Vol 25 (2) ◽  
pp. 61-66 ◽  
Author(s):  
C. Wim Ang ◽  
Bart C. Jacobs ◽  
Jon D. Laman

1993 ◽  
Vol 178 (5) ◽  
pp. 1771-1775 ◽  
Author(s):  
N Yuki ◽  
T Taki ◽  
F Inagaki ◽  
T Kasama ◽  
M Takahashi ◽  
...  

There is a strong association between Guillain-Barré syndrome (GBS) and Penner's serotype 19 (PEN 19) of Campylobacter jejuni. Sera from patients with GBS after C. jejuni infection have autoantibodies to GM1 ganglioside in the acute phase of the illness. Our previous work has suggested that GBS results from an immune response to cross-reactive antigen between lipopolysaccharide (LPS) of the Gram-negative bacterium and membrane components of peripheral nerves. To clarify the pathogenesis of GBS, we have investigated whether GM1-oligosaccharide structure is present in the LPS of C. jejuni (PEN 19) that was isolated from a GBS patient. After extraction of the LPS, the LPS showing the binding activity of cholera toxin, that specifically recognizes the GM1-oligosaccharide was purified by a silica bead column chromatography. Gas-liquid chromatography-mass spectrometric analysis has shown that the purified LPS contained Gal, GalNAc, and NeuAc, which are sugar components of GM1 ganglioside. 1H NMR methods [Carr-Purcell-Meiboom-Gill (CPMG), total correlation spectroscopy (TOCSY), and nuclear Overhauser effect spectroscopy (NOESY)] have revealed that the oligosaccharide structure [Gal beta 1-3 GalNAc beta 1-4(NeuAc alpha 2-3)Gal beta] protrude from the LPS core. This terminal structure [Gal beta 1-3GalNAc beta 1-4(NeuAc alpha 2-3)Gal beta] is identical to the terminal tetrasaccharide of the GM1 ganglioside. This is the first study to demonstrate the existence of molecular mimicry between nerve tissue and the infectious agent that elicits GBS.


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