Innate Immunity to Campylobacter jejuni in Guillain-Barré Syndrome

Autor: 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.
Přispěvatelé: Translational Immunology Groningen (TRIGR), Molecular Neuroscience and Ageing Research (MOLAR)
Jazyk: angličtina
Rok vydání: 2015
Předmět:
Zdroj: Annals of Neurology, 78(3), 343. John Wiley and Sons Inc.
Annals of Neurology, 78(3), 343-354. Wiley
ISSN: 0364-5134
Popis: Objective: Guillain-Barre 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. Methods: 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). Results: 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. Interpretation: 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. Ann Neurol 2015;78:343-354
Databáze: OpenAIRE
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