<i>Campylobacter jejuni</i> infections and anti‐GM1 antibodies in guillain‐barré syndrome

Jacobs, Bart C.; Doorn, Pieter A. van; Tio‐Gillen, Anne P.; Visser, Leo H.; Meché, F. G. A. Van Der; Schmitz, Paul; Herbrink, Paul; Hooijkaas, Herbert

doi:10.1002/ana.410400209

Cited by 301 publications

(215 citation statements)

References 35 publications

(16 reference statements)

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“…It was hypothesized that different sub-types of anti-ganglioside antibodies are associated with different GBS subtypes (35). Anti-GM1 antibodies are commonly associated with a pure motor variant of GBS (36), and GQ1b may be a target antigen responsible for patients with MFS (37). A study reported that anti-ganglioside antibodies are able to inhibit axon regeneration through neuronal gangliosides independent of endogenous regeneration inhibitors (38).…”

Section: Discussionmentioning

confidence: 99%

Toll-like receptor 2 and -4 are involved in the pathogenesis of the Guillain-Barré syndrome

Zhang

et al. 2015

Molecular Medicine Reports

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Abstract. Guillain-Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system characterized by weakness in the limbs. To date, numerous hypotheses have been suggested to explain the pathogenesis of GBS; however, the pathogenesis of GBS remains to be elucidated. The aim of the present study was to investigate the association between Toll-like receptor (TLR) 2, TLR4 and GBS. Therefore, the mRNA of TLR2, TLR4, myeloid differentiation factor (MyD)88 and nuclear factor (NF)-κB of peripheral blood mononuclear cells (PBMCs) in patients with GBS and healthy controls was assessed. To confirm the function of TLR2 and TLR4 in the pathogenesis of GBS, PBMCs derived from patients with GBS and healthy controls were cultured with various TLR agonists. The levels of tumor necrosis factor (TNF)-α and interleukin (IL)-1β were measured in the culture supernatant and fasting serum was obtained for the detection of anti-ganglioside antibodies. The results revealed that the mRNA levels of TLR2, TLR4, MyD88 and NF-κB were significantly increased in patients with GBS compared with those in healthy controls (P=0.003, 0.017, 0.032 and 0.015, respectively). PBMCs from patients with GBS secreted higher levels of TNF-α and IL-1β than those from control subjects. The positive rate of immunoglobulin (Ig)G and IgM anti-ganglioside antibodies in patients with severe GBS was 42.86%, which was markedly higher than rates found in patients with mild GBS (9.09 and 18.18%, respectively). The results of the present study demonstrated that TLR2 and TLR4 are involved in the pathogenesis of GBS and that they and their associated signaling pathways may be targets for the treatment of GBS.

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Section: Discussionmentioning

confidence: 99%

Toll-like receptor 2 and -4 are involved in the pathogenesis of the Guillain-Barré syndrome

Zhang

et al. 2015

Molecular Medicine Reports

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“…Several clinical studies indicate that anti-ganglioside Abs are associated with poor/incomplete recovery (Ilyas et al, 1992;Gregson et al, 1993;Simone et al, 1993;Yuki et al, 1993;Jacobs et al, 1996;Bech et al, 1997;Kuwabara et al, 1998a,b;Carpo et al, 1999;Press et al, 2001;Annunziata et al, 2003;Koga et al, 2003;Kaida et al, 2007). The patients with incomplete recovery almost always have some degree of failure of nerve repair/axon regeneration and target reinnervation (Brown and Feasby, 1984).…”

Section: Discussionmentioning

confidence: 99%

“…The full spectrum of anti-ganglioside Ab-mediated pathobiologic effects and associated mechanisms remain to be defined. Several studies suggest that some GBS patients with anti-ganglioside Abs directed against GM1, GD1a, or ganglioside complexes have poor prognosis and/or incomplete recovery (Ilyas et al, 1992;Gregson et al, 1993;Simone et al, 1993;Yuki et al, 1993;Jacobs et al, 1996;Bech et al, 1997;Kuwabara et al, 1998a,b;Carpo et al, 1999;Press et al, 2001;Annunziata et al, 2003;Koga et al, 2003;Kaida et al, 2007). We recently demonstrated that experimental monoclonal and GBS patient-derived anti-ganglioside Abs can inhibit regeneration of injured axons in an animal model (Lehmann et al, 2007;Lopez et al, 2010), suggesting that Ab-mediated inhibition of nerve repair is one mechanism of delayed recovery.…”

Section: Introductionmentioning

confidence: 97%

Anti-Ganglioside Antibody-Mediated Activation of RhoA Induces Inhibition of Neurite Outgrowth

Zhang¹,

Lehmann

Manoharan

et al. 2011

J. Neurosci.

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Anti-ganglioside antibodies (Abs) are strongly associated with axonal forms of Guillain Barré syndrome (GBS). Some studies indicate that these Abs, including those with GD1a reactivity, are associated with poor prognosis and/or incomplete recovery. We recently demonstrated that a disease-relevant anti-ganglioside Ab with GD1a reactivity inhibits axon regeneration after PNS injury in an animal model (Lehmann et al., 2007). An implication of these findings is that anti-GD1a Abs can mediate inhibition of axon regeneration and limit recovery in some patients with GBS. The downstream inhibitory intracellular signaling that mediates anti-ganglioside Ab-induced axon inhibition remains unclear. In the current study, we show that disease-relevant and GBS patient's anti-ganglioside Abs can inhibit neurite outgrowth in dissociated primary neuronal cultures. Activation of small GTPase RhoA and its key downstream effector Rho kinase (ROCK) are critical mediators of growth cone and neurite outgrowth inhibition. Therefore, we examined the role of these intracellular signaling molecules in our primary neuronal cultures by molecular and pharmacologic approaches. Our results show that the Ab-mediated inhibition of neurite outgrowth involves the activation of RhoA and ROCK pathway and this activation is through the engagement of specific cell-surface gangliosides by Abs. In summary, these studies directly link patient autoantibodies to an intracellular inhibitory signaling pathway involved in anti-ganglioside Abmediated inhibition of neurite outgrowth.

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“…Her neurological symptoms started 1 week later: she consulted her general practitioner because of generalised muscle pain, a rigid neck and a painfully rigid left hand. Routine blood investigations at that moment only showed a slight increase in leucocytes (10 690/mm 3 , reference value 4000-10 000/mm 3 ) and SGPT (28 U/l, reference value o22 U/l). A symptomatic treatment consisting of paracetamol q6h and an intramuscular injection with diclofenac was prescribed.…”

Section: Case Reportmentioning

confidence: 90%

“…3 Acute-phase pretreatment serum contained high titres of anti-GM1 IgG (1:6400) and IgM (1:400) antibodies, which were decreased in a serum sample obtained at 6 months: IgG (1:200) and absent IgM. Both samples were negative for IgG and IgM antibodies to GM2, GM3, GD1a, GD1b, GD2, GD3, GT1a, GT1b and GQ1b.…”

Section: Case Reportmentioning

confidence: 90%

Campylobacter jejuni-induced acute transverse myelitis

et al. 2007

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Case report: Campylobacter jejuni infection is related to various syndromes in which the peripheral nervous system is involved. An immune response is triggered through molecular mimicry between gangliosides of the peripheral nervous system and lipo-oligosaccharides of C. jejuni. We report a case of a previously healthy 17-year-old girl, who developed clinical manifestations of acute transverse myelitis (ATM) 7 days after a culture-proven C. jejuni enteritis. High titres of serum IgG antibodies to the ganglioside GM1 were found in the acute phase of disease, which decreased with clinical recovery. These antibodies cross-reacted with C. jejuni lipo-oligosaccharides, indicating that C. jejuni infections may induce ATM. Conclusions: Only a few cases of C. jejuni infection associated with demyelination of the central nervous system or spinal cord have been described. Physicians should be aware that C. jejuni might be another cause of transverse myelitis. Sponsorship: None.

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Campylobacter jejuni infections and anti‐GM1 antibodies in guillain‐barré syndrome

Cited by 301 publications

References 35 publications

Toll-like receptor 2 and -4 are involved in the pathogenesis of the Guillain-Barré syndrome

Toll-like receptor 2 and -4 are involved in the pathogenesis of the Guillain-Barré syndrome

Anti-Ganglioside Antibody-Mediated Activation of RhoA Induces Inhibition of Neurite Outgrowth

Campylobacter jejuni-induced acute transverse myelitis

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