Innate Immunity to Campylobacter jejuni in Guillain‐Barré Syndrome. Issue 3 (30th June 2015)

• Record Type: Journal Article
• Authors: 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.
• Is Part Of: Annals of neurology. Volume 78:Issue 3(2015:Sep.)
• Page Start: 343
• Page End: 354
• Publication Date: 2015-06-30
• Subjects: Neurology -- Periodicals; Pediatric neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; 616.8
• DOI: 10.1002/ana.24442
• Languages: English
• ISSNs: 0364-5134

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="ana24442-sec-0001" sec-type="section"> <title>Objective</title> <p>Guillain‐Barré syndrome (GBS) is a postinfectious neuropathy most frequently caused by <italic>Campylobacter jejuni</italic>. Lipo‐oligosaccharides (LOS), expressed by <italic>C. jejuni</italic> induce antibodies that cross‐react with self‐glycolipids in peripheral nerves, causing neuropathy. Less than 1 in 1, 000 persons infected with <italic>C. jejuni</italic> 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 <italic>C. jejuni</italic> LOS through Toll‐like receptor 4 (TLR4) activation.</p> </sec> <sec id="ana24442-sec-0002" sec-type="section"> <title>Methods</title> <p>Intrinsic DC responsiveness to <italic>C. jejuni</italic> 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 <italic>C. jejuni</italic> infection (n = 27) and controls (n = 26).</p> </sec> <sec id="ana24442-sec-0003" sec-type="section"> <title>Results</title> <p>The DC response to <italic>C. jejuni</italic> 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 <italic>C. jejuni</italic> 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.</p> </sec> <sec id="ana24442-sec-0004" sec-type="section"> <title>Interpretation</title> <p>These results suggest that a strong response to TLR4 stimulation is a critical host condition for the development of GBS after an infection with <italic>C. jejuni</italic>. Ann Neurol 2015;78:343–354</p> </sec> </abstract>