Publications by authors named "Anne Tio-Gillen"

Article Synopsis
  • A non-pathogenic Mycoplasma pneumoniae is being used to create live biotherapeutic products for treating respiratory diseases, but there are concerns about its connection to Guillain-Barré syndrome (GBS) after infection.
  • Research identified galactolipids, particularly galactocerebroside (GalCer), as likely triggers for autoimmune responses linked to GBS, leading scientists to engineer strains without genes for galactolipid biosynthesis.
  • Some modified strains showed reduced antibody recognition from GBS patients; however, other glycolipids beyond GalCer were also found to influence this recognition, prompting discussions on selecting safe Mycoplasma strains for potential therapeutic use.
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Background And Objectives: Guillain-Barré syndrome (GBS) is an acute immune-mediated polyradiculoneuropathy that may follow a preceding infection inducing a cross-reactive antibody response to glycosphingolipids in peripheral nerves. The immune response in GBS is considered to be short lasting, explaining its monophasic clinical course. However, the disease course varies between patients, and residual deficits frequently occur.

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Article Synopsis
  • Increased Fab glycosylation of autoantibodies is prevalent in chronic B cell-mediated autoimmune diseases, with varying levels found across several conditions including rheumatoid arthritis and systemic lupus erythematosus.
  • Assessment methods included lectin affinity chromatography and autoantigen-specific immunoassays to determine glycosylation levels.
  • The study demonstrated that chronic disease states lead to increased Fab glycosylation, while acute autoimmune diseases did not show this association, suggesting a complex relationship between autoantigen exposure and glycosylation.
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Background And Objectives: Infections play a key role in the development of Guillain-Barré syndrome (GBS) and have been associated with specific clinical features and disease severity. The clinical variation of GBS across geographical regions has been suggested to be related to differences in the distribution of preceding infections, but this has not been studied on a large scale.

Methods: We analyzed the first 1,000 patients included in the International GBS Outcome Study with available biosamples (n = 768) for the presence of a recent infection with , hepatitis E virus, , cytomegalovirus, and Epstein-Barr virus.

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Objective: The Guillain-Barré syndrome (GBS) is an acute, immune-mediated disease of peripheral nerves. Plasmablasts and plasma cells play a central role in GBS by producing neurotoxic antibodies. The standard treatment for GBS is high-dose intravenous immunoglobulins (IVIg), however the working mechanism is unknown and the response to treatment is highly variable.

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We report the case of a 9 year-old boy, presenting with an acute encephalitis with cerebrospinal fluid pleiocytosis. MRI showed T2/FLAIR (fluid attenuated inversion recovery) hyperintense signals of basal ganglia and cortex, EEG (electro encephalogram) showed diffuse slowing with epileptic discharges. A repetitively elevated IgM/IgG serologic response against was observed with polymerase chain reaction in serum and cerebrospinal fluid remaining negative.

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Antibody responses to correlate with pulmonary clearance. However, -specific IgG antibodies can cross-react with the myelin glycolipid galactocerebroside (GalC) and cause neurological disorders. We assessed whether antiglycolipid antibody formation is part of the physiological immune response to We show that antibodies against proteins and glycolipids arise in serum of -infected children and mice.

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Article Synopsis
  • Researchers found that anti-GD1b antibodies are present in some patients with immune-mediated neuropathies, particularly in Guillain-Barré syndrome (GBS) and Miller Fisher-GBS overlap syndrome (MF-GBS).
  • Among various patient groups, IgG anti-GD1b antibodies were primarily observed in GBS (12.1%) and MF-GBS (14.3%), while IgM antibodies were found in lower frequencies.
  • Patients with GBS or MF-GBS harboring only anti-GD1b antibodies showed quicker recovery in their walking ability compared to those with other antibody combinations, indicating potential clinical significance of anti-GD1b testing for diagnosis and treatment planning.
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Mycoplasma pneumoniae (Mp) triggers Guillain-Barré syndrome (GBS) and elicits anti-galactocerebroside (GalC) antibodies. Specifically anti-GalC IgG is associated with Mp-GBS, possibly because of its better ability to cross the blood-nerve barrier (BNB). We here investigated CSF for the presence of anti-GalC in GBS.

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Importance: There is an urgent need for biomarkers to monitor treatment efficacy and anticipate outcome in patients with Guillain-Barré syndrome (GBS).

Objective: To assess whether there is an association between serum albumin levels, a widely used and relatively easily measurable biomarker of health and inflammation, and the clinical course and outcome of GBS in patients treated with intravenous immunoglobulin (IVIG).

Design, Setting, And Participants: We used serum samples derived from a cohort of patients with GBS admitted to hospitals across the Netherlands participating in national GBS studies from May 5, 1986, through August 2, 2000.

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Article Synopsis
  • Guillain-Barré syndrome (GBS) is a serious condition that can happen after infections, and this study looked at how a specific bacteria called Mycoplasma pneumoniae might relate to GBS.
  • Researchers compared blood samples from 189 adults and 24 children with GBS to those from healthy people to see if they had antibodies against the bacteria and a substance called GalC.
  • The findings showed that children with GBS had more chances of having antibodies linked to Mycoplasma pneumoniae and showed signs of more severe symptoms, suggesting that this bacteria might play a role in causing GBS, especially in kids.
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Treatment of Guillain-Barré syndrome with a standard course of high-dose intravenous immunoglobulin (IVIg) results in a variable clinical recovery which is associated with changes in serum IgG levels after treatment. The neonatal Fc-receptor protects IgG from degradation, and a genetic polymorphism in its promoter region that influences the expression of Fc-receptor, may in part explain the variation in IgG levels and outcome. This polymorphism was determined by polymerase chain reaction in a cohort of 257 patients with Guillain-Barré syndrome treated with IVIg.

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Objective: Guillain-Barré syndrome (GBS) is a postinfectious neuropathy most frequently caused by Campylobacter jejuni. Lipo-oligosaccharides (LOS), expressed by C. jejuni induce antibodies that cross-react with self-glycolipids in peripheral nerves, causing neuropathy.

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Monoclonal gammopathy in patients with amyotrophic lateral sclerosis (ALS) and related disorders has been reported in small studies but the validity of the reported associations remains uncertain. Presence of monoclonal gammopathy may indicate specific pathogenic pathways and may facilitate the development of novel treatment strategies. The objective of this large case-control study was to determine the prevalence of monoclonal gammopathy in motor neuron diseases (MND) and multifocal motor neuropathy (MMN).

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Objective: Multifocal motor neuropathy (MMN) and the Guillain-Barré syndrome (GBS) are immune-mediated motor neuropathies with antibodies against the ganglioside GM1. In GBS, these antibodies are induced by molecular mimicry, but in MMN their origin is elusive.

Methods: We compared the light-chain use of anti-GM1 IgM antibodies in serum from 42 patients with MMN and 23 patients with GBS by ELISA.

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Intravenous immunoglobulin (IVIg) is the treatment of choice for Guillain-Barré syndrome (GBS), an immune-mediated peripheral neuropathy causing rapidly progressive limb weakness and respiratory failure. The working mechanism of IVIg in autoimmune diseases has not been elucidated, but previous studies indicate that some anti-inflammatory effects may be mediated by the N-glycosylation of the Fc-portion of IgG. GBS is a model disease to investigate these effects because GBS is an acute and monophasic disorder usually affecting healthy persons, which is treated with a standard course of IVIg, although the clinical response is highly variable.

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IgM antibodies against gangliosides and their complexes were studied in sera from 54 patients with polyneuropathy and IgM monoclonal gammopathy (IgM-PNP) without anti-MAG antibodies. Anti-ganglioside antibodies were found in 19 (35%) patients. Five (9%) patients had antibodies against ganglioside complexes.

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Objective: The aim of the study was to determine whether Guillain-Barré syndrome (GBS) is associated with preceding hepatitis E virus infection.

Methods: The frequency of hepatitis E virus (HEV) infections was determined by anti-HEV serology in a cohort of 201 patients with GBS and 201 healthy controls with a similar distribution in age, sex, and year of sampling. Blood samples from patients with GBS were obtained in the acute phase before treatment.

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Objective: To determine the variability of serum IgG in patients with chronic inflammatory demyelinating polyneuropathy (CIDP).

Methods: All 25 CIDP patients had active but stable disease and were treated with individually optimised fixed dose IVIg regimens. IgG was measured by turbidimetry and variability was defined as coefficient of variation (CV).

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Background: Campylobacter jejuni is the predominant antecedent infection in Guillain-Barré syndrome (GBS). Molecular mimicry and cross-reactive immune responses to C. jejuni lipo-oligosaccharides (LOS) precipitate the development of GBS, although this mechanism has not been established in patients from developing countries.

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Antibodies to the ganglioside GM1 are associated with various forms of acute and chronic immune-mediated neuropathy, including Guillain-Barré syndrome (GBS) and multifocal motor neuropathy. In diagnostics and research, these antibodies are usually detected by GM1 preparations derived from bovine brain tissue, which are non-covalently attached to solid carriers such as enzyme-linked immunosorbent assay (ELISA) plates. Such brain-derived GM1 preparations are potentially contaminated with other glycolipids.

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Monolithic columns containing ganglioside GM2 and GM3 mimics were prepared for selective removal of serum anti-ganglioside antibodies from patients with acute and chronic immune-mediated neuropathies. ELISA results demonstrated that anti-GM2 IgM antibodies in human sera and a mouse monoclonal anti-GM2 antibody were specifically and selectively adsorbed by monolithic GM2 mimic columns and not by blank monolithic columns or monolithic GM3 mimic columns. In control studies, serum antibodies against the ganglioside GQ1b from another neuropathy patient were not depleted by monolithic GM2 mimic columns.

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