• Guillain-Barré syndrome
• anti-ganglioside antibodies
• diagnostic criteria
• electrodiagnosis
• serial examinations

• Humans
• Guillain-Barre Syndrome
• Prospective Studies
• Neural Conduction/physiology
• Electrodiagnosis/methods
• Gangliosides
• Antibodies

• TSA-2020-36889 Scientific Research Projects Coordination Unit of Istanbul University

• Guillain–Barré syndrome
• coronavirus disease 2019
• immunopathogenesis
• polyneuropathy
• therapeutic target

• Guillain-Barre Syndrome/therapy
• Guillain-Barre Syndrome/immunology
• Guillain-Barre Syndrome/physiopathology
• Guillain-Barre Syndrome/drug therapy
• Humans
• COVID-19/immunology
• COVID-19/therapy
• Animals
• Immunoglobulins, Intravenous
• Plasma Exchange/methods
• Immunomodulating Agents/pharmacology
• SARS-CoV-2/immunology

• antimicrobial resistance
• campylobacter jejuni
• identification
• isolation
• prevalence
• risk factors
• sheep

• Humans
• Genetic Predisposition to Disease/genetics
• Guillain-Barre Syndrome/genetics
• Haplotypes
• Interleukin-10/genetics
• Polymorphism, Single Nucleotide
• Promoter Regions, Genetic/genetics

• autoantibodies
• demyelination
• immunity
• inflammation
• neuropathy

• Animals
• Guillain-Barre Syndrome
• Polyradiculoneuropathy, Chronic Inflammatory Demyelinating
• Polyneuropathies
• Autoantibodies
• Inflammation
• Neuritis

• Adhesion
• Antiadhesion
• Campylobacter
• Host–pathogen interaction
• Invasion
• Virulence factors

• Anaerobes
• Autoimmune disease
• Gastro-intestinal tract
• Microbiome
• Microbiota
• Molecular mimicry

• R studio
• dissociation constant
• galectin
• microarray
• python

• T32 GM142617 NIGMS NIH HHS
• National Institutes of Health

• Guillain-Barré syndrome
• allele
• genotype
• nucleotide oligomerization domain
• polymorphism

Four Campylobacter jejuni strains (Z191005RS, Z191005SS, Z201020RS, and Z201020SS) isolated from the axonal variant of Guillain-Barré syndrome (GBS) were sequenced using Illumina technology. The average genome size was from 1.61 to 1.63 gb, with a very high coverage ranging from 654× to 758×, which facilitates the possibility of rare variant calling.

•

Classification of neurophysiologic subtypes of Guillain-Barré syndrome largely depended on the applied criteria.

To describe the electrophysiological features in relation to clinical and serological findings of Guillain-Barré syndrome (GBS) in the national neuroscience hospital in Bangladesh. This is one of the few studies that investigated GBS patients using standardized electrophysiology in low-income countries.

In a prospective and observational study, we investigated 312 GBS patients by standardized clinical, serological and electrophysiological methods. Unilateral motor and sensory nerve conduction studies (NCS) were performed within two weeks of onset of weakness. Follow up NCS were performed in 189 patients and classified according to eight sets of established GBS criteria. Serology included assessment of anti-GM1 antibodies and anti-campylobacter jejuni lipo-oligosaccharide (LOS) antibodies.

Depending on the criteria used, 44–59% patients had axonal GBS with anti-GM1 antibodies being present in 55–58% and 9–42% patients had demyelinating GBS with anti-GM1 antibodies being present in 7–35%. Conduction block (CB) with demyelinative slowing in the same nerve segment was found in 24% (74/312) patients, and CB without demyelinative slowing in the same nerve segment was found in 18% (56/312) patients, of whom anti-GM1 antibodies were found in 27% and 57% patients respectively. Follow-up NCS showed a change in GBS classification in 11–26% of patients, mainly from demyelinating to axonal GBS.

The predominant subtype of GBS in Bangladesh is axonal but demyelinating GBS also occurs with classification being strongly dependent on the applied criteria.

The present study demonstrates the importance of reaching international agreement on GBS criteria that should be based on the best evidence.

• Anti-GM1 antibody
• Axon loss
• Conduction block
• Criteria
• Demyelination
• Guillain-Barré syndrome

• Adhesion
• Diarrhea
• Invasion
• Motility
• Thermophilic campylobacter
• campylobacteriosis

• Adolescent
• Adult
• Anti-Bacterial Agents/pharmacology
• Anti-Bacterial Agents/therapeutic use
• Bangladesh/epidemiology
• Campylobacter/classification
• Campylobacter/drug effects
• Campylobacter/genetics
• Campylobacter/isolation & purification
• Campylobacter Infections/drug therapy
• Campylobacter Infections/epidemiology
• Child
• Child, Preschool
• Diarrhea/microbiology
• Drug Resistance, Multiple, Bacterial
• Female
• Hospitalization
• Humans
• Infant
• Infant, Newborn
• Male
• Middle Aged
• Prevalence
• RNA, Ribosomal, 16S/genetics
• Young Adult

• G B syndrome
• autoimmunity
• axonal degeneration
• demyelination
• peripheral neuropathy
• postinfection

Campylobacter jejuni is the pathogen most commonly associated with Guillain-Barré syndrome (GBS). The present work describes the draft genome sequences of 3 C. jejuni strains, BD39, BD67, and BD75, isolated from stool specimens of C. jejuni-triggered patients with GBS using Illumina technologies.

Campylobacter jejuni is the pathogen most commonly associated with Guillain-Barré syndrome (GBS). The present work describes the draft genome sequences of 3 C. jejuni strains, BD39, BD67, and BD75, isolated from stool specimens of patients with C. jejuni-triggered GBS using Illumina technologies.

• Arbovirus
• Chemokines
• Chikungunya (CHIKV)
• Cytokines
• Dengue (DENV)
• Neurological Complications
• Zika (ZIKV)

• Bangladesh
• Guillain-Barré syndrome
• childhood GBS
• outcome

Campylobacter infection is one of the most common causes of bacterial gastroenteritis worldwide and a major global health threat due to the rapid development of antibiotic resistance. Currently, there are no vaccines approved to prevent campylobacteriosis, and rehydration is the main form of therapy. Secretory immunoglobulin A (SIgA) is the main antibody class found in mucous secretions, including human milk, and serves as the first line of defense for the gastrointestinal epithelium against enteric pathogens. In this study, we describe the prophylactic activity of orally delivered recombinant SIgA generated from two human monoclonal antibodies (CAA1 and CCG4) isolated for their reactivity against the flagellar-capping protein FliD, which is essential for bacteria motility and highly conserved across Campylobacter species associated with severe enteritis. In an immunocompetent weaned mouse model, a single oral administration of FliD-reactive SIgA CAA1 or CCG4 at 2 h before infection significantly enhances Campylobacter clearance at early stages post-infection, reducing the levels of inflammation markers associated with epithelial damage and polymorphonuclear (PMN) cells infiltration in the cecum lamina propria. Our data indicate that the prophylactic activity of CAA1 and CCG4 is not only dependent on the specificity to FliD but also on the use of the SIgA format, as the immunoglobulin G (IgG) versions of the same antibodies did not confer a comparable protective effect. Our work emphasizes the potential of FliD as a target for the development of vaccines and supports the concept that orally administered FliD-reactive SIgA can be developed to prevent or mitigate the severity of Campylobacter infections as well as the development of post-infection syndromes.

• Campylobacter
• FliD
• flagellar-capping protein
• monoclonal antibodies
• prophylaxis
• secretory IgA

Guillain‐Barré syndrome (GBS) is a rare, life‐threatening disorder of the peripheral nervous system. Immunoglobulin G Fc‐gamma receptors (FcγRs) mediate and regulate diverse effector functions and are involved in the pathogenesis of GBS. We investigated whether the FcγR polymorphisms FcγRIIa H/R131 (rs1801274), FcγRIIIa V/F158 (rs396991), and FcγRIIIb NA1/NA2, and their haplotype patterns affect the affinity of IgG‐FcγR interactivity and influence GBS susceptibility and severity.

We determined FcγR polymorphisms in 303 patients with GBS and 302 ethnically matched healthy individuals from Bangladesh by allele‐specific polymerase chain reaction. Pairwise linkage disequilibrium and haplotype patterns were analyzed based on D ´statistics and the genotype package of R statistics, respectively. Logistic regression analysis and Fisher’s exact test with corrected P (Pc) values were employed for statistical comparisons.

FcγRIIIa‐V158F was associated with the severe form of GBS compared to the mild form (P = 0.005, OR = 2.24, 95% CI = 1.28–3.91; Pc = 0.015); however, FcγR genotypes and haplotype patterns did not show any association with GBS susceptibility compared to healthy controls. FcγRIIIa‐V/V158 and FcγRIIIb‐NA2/2 were associated with recent Campylobacter jejuni infection (P ≤ 0.001, OR = 0.36, 95% CI = 0.23–0.56; Pc ≤ 0.003 and P = 0.004, OR = 1.70, 95% CI = 1.18–2.44; Pc ≤ 0.012, respectively). Haplotype 1 (FcγRIIa‐H131R‐ FcγRIIIa‐V158F‐ FcγRIIIb‐NA1/2) and the FcγRIIIb‐NA2/2 genotype were more prevalent among anti‐GM1 antibody‐positive patients (P = 0.031, OR = 9.61, 95% CI = 1.24–74.77, Pc = 0.279; P = 0.027, OR = 1.62, 95% CI = 1.06–2.5, Pc = 0.081, respectively).

FcγR polymorphisms and haplotypes are not associated with susceptibility to GBS, though the FcγRIIIa‐V158F genotype is associated with the severity of GBS.

Genomic composition has been found to be species specific and is used to differentiate bacterial species. To date, almost no published composition-based approaches are able to distinguish between most closely related organisms, including intra-genus species and intra-species strains. Thus, it is necessary to develop a novel approach to address this problem.

Here, we initially determine that the “tetranucleotide-derived z-value Pearson correlation coefficient” (TETRA) approach is representative of other published statistical methods. Then, we devise a novel method called “Tetranucleotide-derived Z-value Manhattan Distance” (TZMD) and compare it with the TETRA approach. Our results show that TZMD reflects the maximal genome difference, while TETRA does not in most conditions, demonstrating in theory that TZMD provides improved resolution. Additionally, our analysis of real data shows that TZMD improves species differentiation and clearly differentiates similar organisms, including similar species belonging to the same genospecies, subspecies and intraspecific strains, most of which cannot be distinguished by TETRA. Furthermore, TZMD is able to determine clonal strains with the TZMD = 0 criterion, which intrinsically encompasses identical composition, high average nucleotide identity and high percentage of shared genomes.

Our extensive assessment demonstrates that TZMD has high resolution. This study is the first to propose a composition-based method for differentiating bacteria at the strain level and to demonstrate that composition is also strain specific. TZMD is a powerful tool and the first easy-to-use approach for differentiating clonal and non-clonal strains. Therefore, as the first composition-based algorithm for strain typing, TZMD will facilitate bacterial studies in the future.

• Composition
• Metagenomic binning
• Species delineation
• Strain typing
• TETRA
• TZMD
• Taxonomy

The etiology of Guillain‐Barré syndrome (GBS) remains enigmatic, although genetic and environmental factors are speculated to be associated with this autoimmune condition. We investigated whether polymorphisms and the haplotype structures of the human leukocyte antigen (HLA)‐DQB1 gene relate to the autoimmune response to infection and affect the development of GBS.

HLA‐DQB1 polymorphic alleles (*0201, *030x, *0401, *050x, *060x) were determined for 151 Bangladeshi patients with GBS and 151 ethnically matched healthy controls using sequence‐specific polymerase chain reaction. Pairwise linkage disequilibrium (LD) and haplotype patterns were analyzed based on D ´statistics and the genotype package in R statistics, respectively. Association studies were conducted using Fisher's exact test and logistic regression analysis. The Bonferroni method was applied to correct for multiple comparisons, whereby the P‐value was multiplied with the number of comparisons and denoted as Pc (Pc, P corrected).

No associations were observed between HLA‐DQB1 alleles and susceptibility to disease in the comparison between GBS patients and healthy subjects. Haplotype 9 (DQB1*0303‐*0601) tended to be less frequent among patients with GBS than healthy controls (P = 0.006, OR = 0.49, 95% CI = 0.30–0.82; Pc = 0.06). Haplotype 5 (DQB1*0501‐*0602) and the DQB1*0201 alleles were more frequent in the Campylobacter jejuni‐triggered axonal variant of GBS (P = 0.024, OR = 4.06, 95% CI = 1.25–13.18; Pc = 0.24) and demyelinating subtype (P = 0.027, OR = 2.68, 95% CI = 1.17–6.17; Pc = 0.35), though these associations were not significant after Bonferroni correction.

This study indicates that HLA‐DQB1 polymorphisms are not associated with susceptibility to GBS. In addition, these genetic markers did not influence the clinical features or serological subgroup in patients with C. jejuni‐triggered axonal variant of GBS.

The bacteria Campylobacter jejuni (C. jejuni) is commonly associated with Guillane-Barré syndrome (GBS) and irritable bowel syndrome (IBS), but studies have also linked it with Miller Fisher syndrome, reactive arthritis and other disorders, some of which are autoimmune. It is possible that C. jejuni and its toxins may be cross-reactive with some human tissues and food antigens, potentially leading to autoimmune responses.

To measure the immune reactivity of C. jejuni and C. jejuni cytolethal distending toxin (Cdt) antibodies with tissue and food antigens to examine their role in autoimmunities.

Using enzyme-linked immunosorbent assay (ELISA) methodology, specific antibodies made against C. jejuni and C. jejuni Cdt were applied to a variety of microwell plates coated with 45 tissues and 180 food antigens. The resulting immunoreactivities were compared to reactions with control wells coated with human serum albumin (HSA) which were used as negative controls and with wells coated with C. jejuni lysate or C. jejuni Cdt which served as positive controls.

At 3 SD above the mean of control wells coated with HSA or 0.41 OD, the mouse monoclonal antibody made against C. jejuni showed moderate to high reactions with zonulin, somatotropin, acetylcholine receptor, β-amyloid and presenilin. This immune reaction was low with an additional 25 tissue antigens including asialoganglioside, and the same antibody did not react at all with another 15 tissue antigens. Examining the reaction between C. jejuni antibody and 180 food antigens, we found insignificant reactions with 163 foods but low to high immune reactions with 17 food antigens. Similarly, we examined the reaction of C. jejuni Cdt with the same tissues and food antigens. The strongest reactions were observed with zonulin, intrinsic factor and somatotropin. The reaction was moderate with 9 different tissue antigens including thyroid peroxidase, and reaction was low with another 10 different antigens, including neuronal antigens. The reaction of C. jejuni Cdt antibody with an additional 23 tissue antigens was insignificant. Regarding the reaction of C. jejuni Cdt antibody with different food antigens, 160 out of 180 foods showed insignificant reactions, while 20 foods showed reactions ranging from low to high.

Our findings indicate that C. jejuni and its Cdt may play a role in inflammation and autoimmunities beyond the gut.

• Campylobacter jejuni
• Cytolethal distending toxin
• Tissue antigens
• Food antigens
• Autoimmune reactivities
• Cross-reactivity

• Antibodies, Bacterial/immunology
• Autoimmune Diseases/immunology
• Autoimmune Diseases/microbiology
• Autoimmunity
• Bacterial Toxins/immunology
• Campylobacter Infections/immunology
• Campylobacter jejuni/immunology
• Cholera Toxin/immunology
• Cross Reactions/immunology
• Dietary Proteins/immunology
• Haptoglobins
• Host Microbial Interactions/immunology
• Human Growth Hormone/immunology
• Humans
• Intrinsic Factor/immunology
• Protein Precursors

TLR4 plays an important role in the pathogenesis of Guillain‐Barré syndrome (GBS). The relationships between TLR4 polymorphisms and susceptibility to GBS are poorly understood. We investigated the frequency and assessed the association of two single nucleotide polymorphisms (SNPs) in the extracellular domain of TLR4 (Asp299Gly and Thr399Ile) with disease susceptibility and the clinical features of GBS in a Bangladeshi cohort.

A total of 290 subjects were included in this study: 141 patients with GBS and 149 unrelated healthy controls. The TLR4 polymorphisms Asp299Gly and Thr399Ile were genotyped using polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) assay.

The minor 299Gly allele was significantly associated with GBS susceptibility (P = 0.0137, OR = 1.97, 95% CI = 1.17–3.31), and was present at a significantly higher frequency in patients with the acute motor axonal neuropathy (AMAN) subtype of GBS (P = 0.0120, OR = 2.37, 95% CI = 1.26–4.47) than acute inflammatory demyelinating polyneuropathy (AIDP) subtype (P = 0.961, OR = 1.15, 95% CI = 0.38–3.48); when compared to healthy controls. The genotype frequency of the Asp299Gly polymorphism was not significantly different between patients with GBS and healthy controls. The Asp299‐Thr399 haplotype was associated with a significantly lower risk of developing GBS (P = 0.0451, OR = 0.63, 95% CI = 0.40–0.99). No association was observed between the Thr399Ile polymorphism and GBS disease susceptibility.

The TLR4 minor 299Gly allele was associated with increased susceptibility to GBS and the axonal GBS subtype in the Bangladeshi population. However, no associations were observed between the genotypes of the Asp299Gly and Thr399Ile SNPs and antecedent C. jejuni infection or disease severity in Bangladeshi patients with GBS.

• Campylobacter jejuni
• biofilm
• cytotoxicity
• hemolysin coregulated protein
• structure

• Anti-Bacterial Agents/isolation & purification
• Anti-Bacterial Agents/therapeutic use
• Bacterial Proteins/genetics
• Bacterial Proteins/metabolism
• Bacterial Vaccines/isolation & purification
• Bacterial Vaccines/therapeutic use
• Campylobacter Infections/genetics
• Campylobacter Infections/metabolism
• Campylobacter Infections/therapy
• Campylobacter jejuni/genetics
• Campylobacter jejuni/growth & development
• Campylobacter jejuni/pathogenicity
• Databases, Protein
• Datasets as Topic
• Drug Discovery/methods
• Genome, Bacterial
• Host-Pathogen Interactions/genetics
• Humans
• Molecular Targeted Therapy/methods
• Signal Transduction/genetics
• Virulence/genetics

• Campylobacter jejuni
• Guillain-Barré syndrome (GBS)
• ganglioside mimicry
• lipooligosaccharide (LOS)
• qPCR
• whole genome sequencing

Zika virus (ZIKV) was initially thought to cause only mild, self-limiting symptoms. However, recent outbreaks have been associated with the autoimmune disease Guillain-Barré syndrome and causally linked to a congenital malformation known as microcephaly. This has led to an urgent need for a safe and effective vaccine. A comprehensive understanding of the immunology of ZIKV infection is required to aid in the design of such a vaccine. Whilst details of both innate and adaptive immune responses to ZIKV are emerging, further research is needed. As immunopathogenesis has been implicated in poor outcomes following infection with the related dengue virus, identification of cross-reactive immune responses between flaviviruses and the impact they may have on disease progression is also of high importance.

• T cells
• Zika virus
• antibodies
• dengue virus
• immunopathogenesis
• innate immunity
• vaccine

Guillain-Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system triggered by molecular mimicry between pathogen lipopolysaccharides and host nerve gangliosides. Polymorphisms in the Fas receptor (FAS) and Fas ligand (FASL) genes may potentially alter the elimination of autoreactive immune cells and affect disease susceptibility or disease severity in GBS. We detected single nucleotide polymorphisms (SNPs) in FAS (-1377G/A and -670A/G) and FASL (-843C/T) in a prospective cohort of 300 patients with GBS and 300 healthy controls from the Bangladeshi population. Genotype distributions were not significantly different between patients with GBS and healthy controls. The FAS -670 AG heterozygous (P = 0.0005, OR = 2.5, 95% CI = 1.5–4.2) and GG homozygous (P = 0.0048, OR = 2.6, 95% CI = 1.3–5.0) genotypes were more common in patients with anti-GM1 antibodies than patients without anti-GM1 antibodies. The FAS -670 G allele was more prevalent in anti-GM1 antibody-positive than -negative patients (P = 0.0002, OR = 1.9, 95% CI = 1.4–2.7) and also in patients with the axonal subtype than demyelinating subtype (P < 0.0001, OR = 4.8, 95% CI = 2.3–10.1). The 1377G/-670G GG haplotype was significantly associated with the axonal subtype (P < 0.0001) and anti-ganglioside antibody-positivity (P = 0.0008) in GBS. Serum sFas (237.5 pg/mL vs. 159.5 pg/mL; P < 0.0001) and sFasL (225.1 pg/mL vs. 183.4 pg/mL; P = 0.0069) were elevated in patients with GBS compared to healthy controls, and among patients with high serum sFas was associated with severe GBS (P = 0.0406). In conclusion, this study indicates FAS-FASL promoter SNPs may promote the production of cross-reactive anti-ganglioside antibodies in GBS.

• Adolescent
• Adult
• Bangladesh
• Case-Control Studies
• Child
• Child, Preschool
• Fas Ligand Protein/genetics
• Female
• G(M1) Ganglioside/immunology
• Guillain-Barre Syndrome/blood
• Guillain-Barre Syndrome/pathology
• Humans
• Male
• Middle Aged
• Peripheral Nervous System/pathology
• Polymorphism, Single Nucleotide
• Promoter Regions, Genetic
• Prospective Studies
• Young Adult
• fas Receptor/blood
• fas Receptor/genetics

• Chicken pox
• Guillain-Barré syndrome
• Herpes zoster
• Shingles
• Varicella zoster virus

Campylobacter jejuni is a major zoonotic pathogen, and its resistance to antibiotics is of great concern for public health. However, few studies have investigated the global changes of the entire organism with respect to antibiotic resistance. Here, we provide mechanistic insights into high-level resistance to chloramphenicol in C. jejuni, using integrated genomic and proteomic analyses. We identified 27 single nucleotide polymorphisms (SNPs) as well as an efflux pump cmeB mutation that conferred modest resistance. We determined two radical S-adenosylmethionine (SAM) enzymes, one each from an SNP gene and a differentially expressed protein. Validation of major metabolic pathways demonstrated alterations in oxidative phosphorylation and ABC transporters, suggesting energy accumulation and increase in methionine import. Collectively, our data revealed a novel rRNA methylation mechanism by a radical SAM superfamily enzyme, indicating that two resistance mechanisms existed in Campylobacter. This work provided a systems biology perspective on understanding the antibiotic resistance mechanisms in bacteria.

• Burden
• Cryptosporidium
• Developing countries
• Diarrhea
• ETEC
• Gastroenteritis
• Rotavirus
• Shigella

• Autoimmunity
• Cytokines
• Guillain-Barre syndrome
• Microcephaly
• Neurodevelopment
• Neurology
• Perinatal infection
• Psychiatry
• Zika virus

• Autoimmunity
• Campylobacter jejuni
• Guillain Barré Syndrome
• Mouse models
• Peripheral neuropathy

• Adult
• Antibodies, Viral/blood
• Antibodies, Viral/cerebrospinal fluid
• Colombia
• Female
• Flavivirus/immunology
• Guillain-Barre Syndrome/etiology
• Humans
• Male
• Middle Aged
• Real-Time Polymerase Chain Reaction
• Zika Virus/genetics
• Zika Virus/isolation & purification
• Zika Virus Infection/complications

• Animals
• Autoantibodies/analysis
• Autoimmune Diseases of the Nervous System/microbiology
• Campylobacter Infections/immunology
• Campylobacter jejuni/immunology
• Cattle/microbiology
• Female
• Food Microbiology
• Gangliosides/immunology
• Humans
• Longitudinal Studies
• Male
• Occupational Exposure/analysis
• Occupational Exposure/statistics & numerical data
• Peripheral Nervous System Diseases/immunology
• Peripheral Nervous System Diseases/microbiology
• Poultry/microbiology
• Swine/microbiology

• R01 NS054962 NINDS NIH HHS
• R01 NS042888 NINDS NIH HHS
• Z01-ES049030 NIEHS NIH HHS
• Z01 ES049030 Intramural NIH HHS
• T42OH008428 NIOSH CDC HHS
• T42OH008428 ACL HHS

• Australia
• Guillain-Barré syndrome
• acute inflammatory demyelinating polyradiculoneuropathy
• epidemiology
• seasonal variation

Ganglioside as a neurotrophic drug has been hitherto widely used in China, although Guillain-Barré syndrome (GBS) following intravenous ganglioside treatment was reported in Europe several decades ago. We identified 7 patients who developed GBS after intravenous use of gangliosides (ganglioside+ group) and compared their clinical data with those of 77 non-ganglioside-associated GBS patients (ganglioside− group) in 2013, aiming at gaining the distinct features of ganglioside-associated GBS. Although the mean age, protein levels in cerebrospinal fluid (CSF) and frequency of cranial nerve involvement were similar between the two groups, the Hughes Functional Grading Scale (HFGS) score and the Medical Research Council (MRC) sum score at nadir significantly differed (4.9±0.4 vs 3.6±1.0; 7.7±5.5 vs 36.9±14.5, both p<0.001), indicating a higher disease severity of ganglioside-associated GBS. A higher ratio of patients with ganglioside-associated GBS required mechanical ventilation (85.7% vs 15.6%, p<0.01). The short-term prognosis of ganglioside-associated GBS, as measured by the HFGS score and the MRC sum score at discharge, was poorer (4.3±0.5 vs 2.8±1.1; 17.3±12.9 vs 46.0±13.9, both p<0.001). All the patients in the ganglioside+ group presented an axonal form of GBS, namely acute motor axonal neuropathy (AMAN). When compared with the AMAN patients in the ganglioside− group, more severe functional deficits at nadir and poorer recovery after standard treatment were still prominent in ganglioside-associated GBS. Anti-GM1 and anti-GT1a antibodies were detectable in patients with AMAN while not in patients with the demyelinating subtype of GBS. The concentrations of these antibodies in patients with AMAN were insignificantly different between the ganglioside+ and ganglioside− groups. In sum, ganglioside-associated GBS may be a devastating side effect of intravenous use of gangliosides, which usually manifests a more severe clinical course and poorer outcome.

• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Antibodies/blood
• Antibodies/cerebrospinal fluid
• Axons/pathology
• China
• Demography
• Electrophysiological Phenomena
• Female
• Gangliosides/adverse effects
• Gangliosides/immunology
• Guillain-Barre Syndrome/blood
• Guillain-Barre Syndrome/cerebrospinal fluid
• Guillain-Barre Syndrome/chemically induced
• Guillain-Barre Syndrome/pathology
• Humans
• Male
• Middle Aged
• Prognosis
• Time Factors
• Young Adult

• campylobacter jejuni
• colitis
• t cells
• guillain barré syndrome (gbs)

• Amino Acid Substitution/genetics
• Campylobacter jejuni/drug effects
• Campylobacter jejuni/genetics
• Campylobacter jejuni/growth & development
• Chloramphenicol/pharmacology
• Drug Resistance, Bacterial/drug effects
• Drug Resistance, Bacterial/genetics
• Kinetics
• Mutation/genetics
• RNA, Ribosomal, 23S/genetics
• Thiamphenicol/analogs & derivatives
• Thiamphenicol/pharmacology

Cross-reactive antibodies are characterized by their recognition of antigens that are different from the trigger immunogen. This happens when the similarity between two different antigenic determinants becomes adequate enough to enable a specific binding with such cross-reactive antibodies. In the present manuscript, we report the presence, at an “abnormal” high frequency, of antibodies in blood samples from French human subjects cross-reacting with a synthetic-peptide antigen derived from a Trypanosoma cruzi (T. cruzi) protein sequence. As the vector of T. cruzi is virtually confined to South America, the parasite is unlikely to be the trigger immunogen of the cross-reactive antibodies detected in France. At present, the cross-reactive antibodies are measured by using an in-house ELISA method that employs the T. cruzi -peptide antigen. However, to underline their cross-reactive characteristics, we called these antibodies “Trypanosoma cruzi Cross Reactive Antibodies” or TcCRA. To validate their cross-reactive nature, these antibodies were affinity-purified from plasma of healthy blood donor and were then shown to specifically react with the T. cruzi parasite by immunofluorescence. Seroprevalence of TcCRA was estimated at 45% in serum samples of French blood donors while the same peptide-antigen reacts with about 96% of T. cruzi -infected Brazilian individuals. In addition, we compared the serology of TcCRA to other serologies such as HSV 1/2, EBV, HHV-6, CMV, VZV, adenovirus, parvovirus B19, mumps virus, rubella virus, respiratory syncytial virus, measles and enterovirus. No association was identified to any of the tested viruses. Furthermore, we tested sera from different age groups for TcCRA and found a progressive acquisition starting from early childhood. Our findings show a large seroprevalence of cross-reactive antibodies to a well-defined T. cruzi antigen and suggest they are induced by a widely spread immunogen, acquired from childhood. The etiology of TcCRA and their clinical relevance still need to be investigated.

• Adolescent
• Adult
• Aged
• Aged, 80 and over
• Amino Acid Sequence
• Antibodies, Protozoan/immunology
• Antigens, Protozoan/immunology
• Antigens, Viral/chemistry
• Antigens, Viral/immunology
• Blood Donors
• Chagas Disease/immunology
• Child
• Child, Preschool
• Cross Reactions/immunology
• Female
• France/epidemiology
• Humans
• Infant
• Infant, Newborn
• Male
• Middle Aged
• Molecular Sequence Data
• Peptides/chemistry
• Peptides/immunology
• Sequence Alignment
• Seroepidemiologic Studies
• Trypanosoma cruzi/immunology
• Viruses/classification
• Viruses/immunology
• Young Adult

• Campylobacter jejuni/genetics
• Gene Transfer, Horizontal/genetics
• Genetic Variation/genetics
• Genome, Bacterial/genetics
• Phylogeny