Autor(es): Huizinga Ruth; van den Berg Bianca; van Rijs Wouter; Tio-Gillen Anne P.; Fokkink Willem Jan R.; Bakker-Jonges Liesbeth E.; Geleijns Karin.; Samsom Janneke N.; van Doorn Pieter A.; Laman Jon D.; Jacobs Bart C.;

Resumo: 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. Less than 1 in 1,000 persons infected with C. jejuni develop GBS, and the factors that determine GBS susceptibility are poorly understood. We hypothesized that these persons have a high intrinsic dendritic cell (DC) response to C. jejuni LOS through Toll-like receptor 4 (TLR4) activation. Intrinsic DC responsiveness to C. jejuni LOS was investigated first in 20 healthy controls at three time points with a 3-month interval, and second in patients, who previously developed GBS after a C. jejuni infection (n = 27) and controls (n = 26). The DC response to C. jejuni LOS was highly variable between, but not within, healthy individuals, suggesting that intrinsic factors determine the magnitude of TLR4-mediated innate response. High responsiveness to C. jejuni LOS by former GBS patients was evidenced by increased expression of CD38 and CD40. Frequency of CD38, CD40 and type I interferon high responders was significantly increased in the GBS group. These results suggest that a strong response to TLR4 stimulation is a critical host condition for the development of GBS after an infection with C. jejuni.

Imprenta: Annals of Neurology, v. 78, n. 3, p. 343-354, 2015

Identificador do objeto digital: 10.1002/ana.24442

Descritores: Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Antibodies ; Guillain-Barre Syndrome - Epidemiology ; Guillain-Barre Syndrome - Immunology ; Guillain-Barre Syndrome - Public health

Data de publicação: 2015

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