Characterization of Campylobacter jejuni isolates from patients with Guillain-Barré syndrome

Nishimura, Masataka; Nukina, Masafumi; Kuroki, Shigekazu; Obayashi, Hiroshi; Ohta, Mitsuhiro; Jun, Jian; Saida, Takahiko; Uchiyama, Takashi

doi:10.1016/s0022-510x(97)00170-6

Cited by 29 publications

(21 citation statements)

References 36 publications

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“…C. jejuni has been isolated from patients' stools at GBS onset. (5), but Kuroki's group showed that 75% of 16 isolates from GBS patients were HS:19 and that 1 of 2 isolates from FS patients was HS:2 (22). Elsewhere we reported that in Japan HS:19 strains are significantly over-represented in GBS patients, accounting for 52% of 31 isolates from GBS patients but only 5% of 215 control isolates (34).…”

Section: Vol 43 2005mentioning

confidence: 62%

Epidemiology ofCampylobacter jejuniIsolated from Patients with Guillain-Barré and Fisher Syndromes in Japan

et al. 2005

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Campylobacter jejuni isolation is the standard for the diagnosis of this type of bacterial infection, but there have been no epidemiological studies of a large number of C. jejuni isolates from patients with Guillain-Barré syndrome (GBS) and Fisher syndrome (FS). For 13 years, stool specimens from GBS/FS patients have been sent from 378 hospitals throughout Japan to the Tokyo Metropolitan Institute of Public Health. A total of 113 strains (11%) were isolated from the stool specimens from 1,049 patients. The isolation rate did not differ by region. The rates were 22% for 449 patients with a history of diarrhea and 2% for the others. An additional 18 isolates were provided by various hospitals. There was no noticeable seasonal distribution in the onset of C. jejuni isolated from patients with GBS/FS. The male/female ratios were 1.7:1 for GBS and 2.2:1 for FS. The patient age range showed a peak in 10-to 30-year-old subjects who had GBS and in 10-to 20-year-old subjects who had FS. The predominance of young adults and male patients who had C. jejuni-associated GBS/FS may be related to the preponderance of young adults and male patients who had C. jejuni enteritis. The median interval from diarrhea onset to neurologic symptom onset was 10 days for GBS/FS. Penner's C. jejuni serotype HS:19 was more frequently present in GBS (67%) than in enteritis (6%) patients. HS:2 was more frequent in FS (41%) than in enteritis (14%) patients. These findings suggest that certain C. jejuni strains specifically trigger GBS and that others specifically trigger FS.

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Section: Vol 43 2005mentioning

confidence: 62%

Epidemiology ofCampylobacter jejuniIsolated from Patients with Guillain-Barré and Fisher Syndromes in Japan

et al. 2005

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“…There is evidence that epitope recognition by molecular mimicry expands to multiple cross-reactivity (epitope spreading) [34]. Anti-GM1 antibody production in patients with GBS after an antecedent C. jejuni infection is associated with carbohydrate mimicry between the oligosaccharides of GM1 and LPS [9,10]. Direct evidence has been provided by sensitizing Lewis rats with the LPS of C. jejuni HS 19, which results in the subsequent elevation of antibody titers against GM1 and GD3 in the sera of these animals [35].…”

Section: Discussionmentioning

confidence: 99%

“…Campylobacter jejuni (C. jejuni) is a gram-negative bacterium expressing two components of strain-specific lipooligosaccharides (LOSs), a lipid A (or endotoxin) portion and a polysaccharide portion [7,8]. Molecular mimicry between the carbohydrate structures of GM1 and of LOS derived from the serotype HS19 of C. jejuni is presumed to be a trigger for antibody production [9,10]. We found that the LOS from strain HS19 of C. jejuni was composed of two distinct components distinguishable by the TLCoverlay profile to cholera toxin binding; these components are provisionally designated as fastand slow-moving bands (LF and LS) based on their mobility on the TLC plate.…”

Section: Introductionmentioning

confidence: 99%

Chemical validation of molecular mimicry: interaction of cholera toxin with Campylobacter lipooligosaccharides

et al. 2007

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It is generally believed that molecular mimicry between bacterial lipooligosaccharide (LOS) and nerve glycolipids may play an important pathogenic role in immune-mediated peripheral neuropathy. One of the putative infectious agents is Campylobacter jejuni (C. jejuni). To elucidate the structural basis for the molecular mimicry, we investigated the structure of the lipooligosaccharide (LOS) fraction of C. jejuni, strain HS19, and found that it includes at least two components, characterized as fast-and slow-moving bands (LF and LS) by thin-layer chromatography as revealed by cholera toxin B subunit (Ctxb) overlay. Structural analysis of the oligosaccharide portion of LS established that it had the following structure: Gal-GalNAc-(NeuAc)Gal-Hep-(Glc;PO 3 H)Hep-Kdo. The GM1-like epitope was validated by a terminal tetrasaccharide unit within this structure. On the other hand, analysis of LF revealed an entirely different structure: 1, 4′-bisphosphoryl glucosamine disaccharide N, N'-acylated by 3-(2-hydroxytetracosanoyloxy)octadecanoic acid at 2-and 2′-positions, which is consistent with that of lipid A. No GM1-like epitope was observed in LF. Both LS and LF interacted with Ctxb as demonstrated by TLC-overlay and sucrose density gradient centrifugation. Surprisingly, LF does not have the basic GM1 structure for interacting with Ctxb. Instead, the affinity of LF to Ctxb required that one or both of the phosphate groups be present in the glucosamine disaccharide residue because after alkaline phosphatase treatment the dephosphorylated LF was unable to bind to Ctxb. We conclude that LS is likely the component contributing to GM1-mimicry in autoimmune peripheral neuropathy and that the role of LF is not clear but may be associated with the initial activation of autoreactive T cells.

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“…In light of the wide occurrence of anti-GSL Abs in these patients, recent research on GBS has focused on GSL mimicry between LPSs in C. jejuni and endogenous GSLs in the peripheral nervous system that may be involved in the pathological mechanisms of GBS (Ang et al, 2004). Strain HS19 of C. jejuni was isolated from GBS patients and paralytic chickens (Li et al, 1996) and found to be associated with 29% of C. jejuniassociated GBS patients in the United States and 83% of cases in Japan (Nishimura et al, 1997;Allos et al, 1998). Although GSL mimicry as a causative mechanism remains uncertain for GBS and related diseases, the terminal tetrasaccharides Galβ1-3GalNAcβ1-4(NeuAcα2-3) Galβ1-4 of a GM1-like epitope and NeuAcα2-8NeuAcα2-3Galβ1-4Hep of a GD3-like epitope have been chemically determined in the LPSs from HS19 (Aspinall et al, 1992(Aspinall et al, , 1994Yuki et al, 1993).…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Molecular mimicry: Sensitization of Lewis rats with Campylobacter jejuni lipopolysaccharides induces formation of antibody toward GD3 ganglioside

Usuki

Thompson

Rivner

et al. 2005

J of Neuroscience Research

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Recently we have reported cases of demyelinating inflammatory neuropathy showing elevated titers of anti-GD3 antibodies, which occurs rarely in Guillain-Barré syndrome. To examine the correlation between the anti-GD3 antibody titer and Campylobacter jejuni infection, we sensitized female Lewis rats with lipopolysaccharides (LPSs) from serotype HS19 of C. jejuni and examined changes in nerve conduction velocity and nerve conduction block (P/D ratio). After 16 weeks of sensitization, animals revealed decreases of nerve conduction velocity and conduction block (P/D ratio) and high titer of anti-GD3 antibodies. These anti-GD3 antibodies also blocked transmission in neuromuscular junctions of spinal cord-muscle cells cocultures. The GD3 epitope was verified to be located on the Schwann cell surface and nodes of Ranvier in rat sciatic nerve. To determine the target epitope for GD3 antibodies in causing nerve dysfunction, the LPS fraction containing the GD3 epitope was purified from the total LPS by using an anti-GD3 monoclonal antibody-immobilized affinity column. Subsequently, chemical analysis of the oligosaccharide portion was performed and confirmed the presence of a GD3-like epitope as having the following tetrasaccharide structure: NeuAcα2-8NeuAc2-3Galβ1-4Hep. Our data thus support the possibility of a contribution of GD3 mimicry as a potential pathogenic mechanism of peripheral nerve dysfunction. Keywordsganglioside; Guillain-Barré; syndrome; anti-ganglioside antibody; GD3; Campylobacter jejuni; LPS Guillain-Barré syndrome (GBS) is an acute immune-mediated peripheral neuropathy consisting of acute inflammatory demyelinating polyneuropathy (AIDP), acute motor neuropathy (AMAN), and related disorders. Anti-GM1 antibodies are often detected in patients with AIDP and AMAN (Kornberg et al., 1994;Arasaki et al., 1998;Hiraga et al., 2005). Many investigators have reported the association between an antecedent Campylobacter jejuni (C. jejuni) infection and subsequent development of GBS. The lipopolysaccharides (LPSs) of a certain serotype of C. jejuni have been shown to possess carbohydrate epitopes similar to *Correspondence to: Dr. Robert K. Yu, Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912-2697. ryu@mcg.edu. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript gangliosides, which may serve as the putative pathogenic triggers for subsequent GBS onset. Thus, these disorders may develop as a result of C. jejuni infection. In addition to anti-GQ1b Abs, anti-GD3 Abs have been detected in the Miller Fisher variant of GBS (Chiba et al., 1992;Carpo et al., 1998;Susuki et al., 2001;Willison and Yuki, 2002;Willison et al., 2004).Recently we have reported cases of AIDP and chronic inflammatory demyelinating polyneuropathy (CIDP) showing high elevations of anti-GD3 Abs, which rarely occurs in GBS (Usuki et al., 2005). The question then arises of the origin of the antiglycolipid (anti-GSL) Abs in GBS, in particular, the mechanism of el...

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Characterization of Campylobacter jejuni isolates from patients with Guillain-Barré syndrome

Cited by 29 publications

References 36 publications

Epidemiology ofCampylobacter jejuniIsolated from Patients with Guillain-Barré and Fisher Syndromes in Japan

Epidemiology ofCampylobacter jejuniIsolated from Patients with Guillain-Barré and Fisher Syndromes in Japan

Chemical validation of molecular mimicry: interaction of cholera toxin with Campylobacter lipooligosaccharides

Molecular mimicry: Sensitization of Lewis rats with Campylobacter jejuni lipopolysaccharides induces formation of antibody toward GD3 ganglioside

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