scholarly journals Molecular Mimicry inCampylobacter jejuniLipopolysaccharides and the Development of Guillain‐Barré Syndrome

1998 ◽  
Vol 178 (5) ◽  
pp. 1549-1550 ◽  
Author(s):  
Anthony P. Moran ◽  
Martina M. Prendergast
Keyword(s):  
Molecular Mimicry ◽  
Guillain Barre Syndrome ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

scholarly journals Guillain-Barré Syndrome and Campylobacter jejuni Infection: A Review

2014 ◽  
Vol 2 (1) ◽  
pp. 28-35 ◽  
Author(s):  
Nurun Nahar Mawla ◽  
Shahin Sultana ◽  
Nayareen Akhter
Keyword(s):  
Campylobacter Jejuni ◽  
Peripheral Nerves ◽  
Molecular Mimicry ◽  
Serum Antibody ◽  
Guillain Barre Syndrome ◽  
Recent Infection ◽  
Culture Studies ◽  
Guillain Barré Syndrome ◽  
Guillain Barré ◽  
Campylobacter Infection

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

scholarly journals Guillain–Barré syndrome: pathophysiology, etiology, causes, and treatment

2021 ◽  
Author(s):  
Rahmathulla S. Rahman ◽  
Moayyad S. Bauthman ◽  
Amer M. Alanazi ◽  
Naif N. Alsillah ◽  
Ziyad M. Alanazi ◽  
...  
Keyword(s):  
Literature Review ◽  
Peripheral Nerves ◽  
Neuromuscular Junctions ◽  
Molecular Mimicry ◽  
Intravenous Immunoglobulins ◽  
Guillain Barre Syndrome ◽  
Gastrointestinal Infections ◽  
Serious Adverse Events ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

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. 

scholarly journals The Development of Guillain Barre Syndrome Subsequent to Administration of Ad26.COV2.S Vaccine

2021 ◽  
pp. 1-3
Author(s):  
Rachel Koreen ◽  
◽  
Jacob Chevlen DO ◽  
Keyword(s):  
Nervous System ◽  
Respiratory Failure ◽  
Molecular Mimicry ◽  
Asymptomatic Infection ◽  
Guillain Barre Syndrome ◽  
Neurologic Disorder ◽  
Diagnostic Certainty ◽  
Guillain Barré Syndrome ◽  
Level 3 ◽  
Guillain Barré

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

The Guillain–Barré syndrome: a true case of molecular mimicry

2004 ◽  
Vol 25 (2) ◽  
pp. 61-66 ◽  
Author(s):  
C. Wim Ang ◽  
Bart C. Jacobs ◽  
Jon D. Laman
Keyword(s):  
Molecular Mimicry ◽  
Guillain Barre Syndrome ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

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
Keyword(s):  
Molecular Mimicry ◽  
Guillain Barre Syndrome ◽  
Igg Antibodies ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

scholarly journals A bacterium lipopolysaccharide that elicits Guillain-Barré syndrome has a GM1 ganglioside-like structure.

1993 ◽  
Vol 178 (5) ◽  
pp. 1771-1775 ◽  
Author(s):  
N Yuki ◽  
T Taki ◽  
F Inagaki ◽  
T Kasama ◽  
M Takahashi ◽  
...  
Keyword(s):  
Molecular Mimicry ◽  
Correlation Spectroscopy ◽  
Nerve Tissue ◽  
Guillain Barre Syndrome ◽  
Spectrometric Analysis ◽  
Gas Liquid Chromatography ◽  
Gm1 Ganglioside ◽  
Oligosaccharide Structure ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

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.

scholarly journals Zika E Glycan Loop Region and Guillain–Barré Syndrome-Related Proteins: A Possible Molecular Mimicry to Be Taken in Account for Vaccine Development

Vaccines ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 283
Author(s):  
Grégorie Lebeau ◽  
Etienne Frumence ◽  
Jonathan Turpin ◽  
Floran Begue ◽  
Jean-Jacques Hoarau ◽  
...  
Keyword(s):  
Heat Shock ◽  
Autoimmune Diseases ◽  
Vaccine Development ◽  
Molecular Mimicry ◽  
Viral Envelope ◽  
Guillain Barre Syndrome ◽  
Loop Region ◽  
E Protein ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

The neurological complications of infection by the mosquito-borne Zika virus (ZIKV) include Guillain–Barré syndrome (GBS), an acute inflammatory demyelinating polyneuritis. GBS was first associated with recent ZIKV epidemics caused by the emergence of the ZIKV Asian lineage in South Pacific. Here, we hypothesize that ZIKV-associated GBS relates to a molecular mimicry between viral envelope E (E) protein and neural proteins involved in GBS. The analysis of the ZIKV epidemic strains showed that the glycan loop (GL) region of the E protein includes an IVNDT motif which is conserved in voltage-dependent L-type calcium channel subunit alpha-1C (Cav1.2) and Heat Shock 70 kDa protein 12A (HSP70 12A). Both VSCC-alpha 1C and HSP70 12A belong to protein families which have been associated with neurological autoimmune diseases in central nervous system. The purpose of our in silico analysis is to point out that IVNDT motif of ZIKV E-GL region should be taken in consideration for the development of safe and effective anti-Zika vaccines by precluding the possibility of adverse neurologic events including autoimmune diseases such as GBS through a potent mimicry with Heat Shock 70 kDa protein 12A (HSP70 12A).

Intracerebral haemorrhage and Guillain-Barré syndrome: an exploration of potential pathophysiology

2021 ◽  
Vol 14 (8) ◽  
pp. e243245
Author(s):  
Sophia Connor ◽  
Omar Azzam ◽  
David Prentice
Keyword(s):  
Differential Diagnosis ◽  
Intracerebral Haemorrhage ◽  
Molecular Mimicry ◽  
Guillain Barre Syndrome ◽  
Important Differential Diagnosis ◽  
Immune Mediated ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

Guillain-Barré syndrome (GBS) is an immune-mediated polyneuropathy classically thought to be caused by infections through the process of molecular mimicry. We report a case of GBS caused by intracerebral haemorrhage and postulate potential theories for the development of GBS following intracerebral haemorrhage and other non-infectious aetiologies by association. We highlight that GBS is an important differential diagnosis in patients developing generalised paresis following intracerebral haemorrhage.

Guillain-Barré Syndrome Variant presenting as Acute Descending Paralysis in Diabetes

2020 ◽  
Vol 2 (1) ◽  
pp. 1-2
Author(s):  
Sumesh Raj ◽  
Manoj Parameswaran
Keyword(s):  
Molecular Mimicry ◽  
Radicular Pain ◽  
Guillain Barre Syndrome ◽  
Gastrointestinal Dysfunction ◽  
Common Features ◽  
High Clinical Suspicion ◽  
Immune Mediated ◽  
Guillain Barré Syndrome ◽  
Diagnostic Modalities ◽  
Guillain Barré

Guillain-Barré Syndrome (GBS) is an acute monophasic immune-mediated polyradiculopathy. Neuropathic or radicular pain and dysautonomia are common features in all forms of GBS. Phenotypic variants are hypothesized to be mediated by molecular mimicry targeting peripheral nerve motor axons, with resulting weakness deviating from the classic symmetric “ascending” pattern. Weakness can range from mild to severe flaccid quadriplegia and respiratory failure within days of onset. Urinary retention and gastrointestinal dysfunction are seen in approximately 5% of variant cases. A spectrum of clinical features necessitates the use of laboratory testing and diagnostic modalities to exclude mimics and confirm a diagnosis of GBS. A high clinical suspicion must exist as GBS responds to treatment with plasmapheresis or IVIG. Our patient embodied both a diagnostically challenging presentation and clinical response consistent with variant GBS.

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