Guillain-Barré syndrome associated with IgM anti-GM1 antibody followingCampylobacter jejuni enteritis

Sugita, Katsuo; Ishii, Motoyasu; Takanashi, Jun‐ichi; Niimi, Hiroo; Yuki, Nobuhiro

doi:10.1007/bf01958981

Cited by 5 publications

(2 citation statements)

References 24 publications

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“…Our patients with CAGBS were younger than those previously described, with the exception of the patients reported by De Bont et al (2 years)3 and Sugita et al (4 years) 5. Patients reported by Kuroki et al were aged 7–14 years (median 11 years),4 whereas Yuki et al reported two patients aged 13 and 9 years with Miller-Fisher syndrome associated with campylobacter 14…”

Section: Discussioncontrasting

confidence: 51%

Campylobacter 0:41 isolation in Guillain-Barre syndrome

Goddard

Lastovica

Argent

1997

Archives of Disease in Childhood

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Section: Discussioncontrasting

confidence: 51%

Campylobacter 0:41 isolation in Guillain-Barre syndrome

Goddard

Lastovica

Argent

1997

Archives of Disease in Childhood

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“…In severe cases, axonal degeneration may accompany the demyelination. Less frequently encountered in North America and Europe but common in China (50,100), Japan (152,175,185,186), Mexico (126), and probably other regions of world are the axonal patterns, in which axons appear to be the target of the immune attack.…”

Section: Gbsmentioning

confidence: 99%

CampylobacterSpecies and Guillain-Barré Syndrome

1998

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SUMMARY Since the eradication of polio in most parts of the world, Guillain-Barré syndrome (GBS) has become the most common cause of acute flaccid paralysis. GBS is an autoimmune disorder of the peripheral nervous system characterized by weakness, usually symmetrical, evolving over a period of several days or more. Since laboratories began to isolate Campylobacter species from stool specimens some 20 years ago, there have been many reports of GBS following Campylobacter infection. Only during the past few years has strong evidence supporting this association developed. Campylobacter infection is now known as the single most identifiable antecedent infection associated with the development of GBS. Campylobacter is thought to cause this autoimmune disease through a mechanism called molecular mimicry, whereby Campylobacter contains ganglioside-like epitopes in the lipopolysaccharide moiety that elicit autoantibodies reacting with peripheral nerve targets. Campylobacter is associated with several pathologic forms of GBS, including the demyelinating (acute inflammatory demyelinating polyneuropathy) and axonal (acute motor axonal neuropathy) forms. Different strains of Campylobacter as well as host factors likely play an important role in determining who develops GBS as well as the nerve targets for the host immune attack of peripheral nerves. The purpose of this review is to summarize our current knowledge about the clinical, epidemiological, pathogenetic, and laboratory aspects of campylobacter-associated GBS.

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Evaluation of Cytokine Production and Phagocytic Activity in Mice Infected with Campylobacter jejuni

Pancorbo

Pablo

Ortega

et al. 1999

Current Microbiology

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The effect of several Campylobacter jejuni strains on the immune response was analyzed in mice after intraperitoneal inoculation with 10(10) colony forming units (CFU). Three C. jejuni strains were assayed: CCUG 6968 (enterotoxigenic), CCUG 7580 (enterotoxigenic), and CCUG 7440 (non-enterotoxigenic). These C. jejuni strains induced a peritoneal inflammatory response and an important increase in the peritoneal phagocyte oxidative activity measured by chemiluminescence assay, as well as an increase in the number of peritoneal cells. Both interleukin-1 (IL-1) and tumor necrosis factor alpha (TNFalpha) production by peritoneal cells were not modified. However, C. jejuni 7440 caused a statistically significant increase in TNFalpha production. These results have demonstrated that different strains of C. jejuni induce an increase of the inflammatory response without a significant cytokine release. However, these infectious microorganisms may be eliminated efficiently by murine macrophages after phagocytosis.

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Guillain-Barré syndrome associated with IgM anti-GM1 antibody followingCampylobacter jejuni enteritis

Cited by 5 publications

References 24 publications

Campylobacter 0:41 isolation in Guillain-Barre syndrome

Campylobacter 0:41 isolation in Guillain-Barre syndrome

CampylobacterSpecies and Guillain-Barré Syndrome

Evaluation of Cytokine Production and Phagocytic Activity in Mice Infected with Campylobacter jejuni

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