Intrathecal immunoreactivity in people with or without previous infectious mononucleosis.
Adolescent
Adult
Biomarkers
/ cerebrospinal fluid
Cohort Studies
Cytokines
/ cerebrospinal fluid
Female
Humans
Infectious Mononucleosis
/ cerebrospinal fluid
Inflammation Mediators
/ cerebrospinal fluid
Interleukin-1beta
/ cerebrospinal fluid
Male
Middle Aged
Multiple Sclerosis
/ cerebrospinal fluid
Tumor Necrosis Factor-alpha
/ cerebrospinal fluid
Young Adult
Epstein-Barr virus
endophenotype
infectious mononucleosis
multiple sclerosis
presymptomatic
Journal
Acta neurologica Scandinavica
ISSN: 1600-0404
Titre abrégé: Acta Neurol Scand
Pays: Denmark
ID NLM: 0370336
Informations de publication
Date de publication:
Aug 2020
Aug 2020
Historique:
received:
21
02
2020
revised:
07
05
2020
accepted:
12
05
2020
pubmed:
18
5
2020
medline:
27
10
2020
entrez:
17
5
2020
Statut:
ppublish
Résumé
The risk of developing multiple sclerosis (MS) increases (OR: 3.1) after infectious mononucleosis (IM). However, the nature of this link is obscure. We tested the hypothesis that IM might incur long-term sequelae, including low-key inflammatory activity, with characteristics of an MS endophenotype (or presymptomatic trait) and that assays of MS-relevant cyto-/chemokines in the cerebrospinal fluid (CSF) post-IM may show a trend in this direction. We selected seven CSF cytokines (IL-1b, IL-6, YKL-40, TNF-alpha) or chemokines (IL-8, CCL2, IP-10), representing pro-inflammatory factors previously associated with MS. We assayed the CSF levels of these seven cyto-/chemokines in healthy individuals with a median follow-up time of 10 years after serologically confirmed IM (post-IM group, n = 22), and in healthy controls without a history of IM (n = 19). A group of MS patients (n = 23) were included as reference. The CSF levels of IP-10, YKL-40, and CCL-2 were higher in the post-IM group than in our IM unexposed controls (P = .021, .049, .028). Seven of seven cyto-/chemokine assays showed a trend in the predicted direction (P of binomial ratio = .008). However, this trend was non-significant in a multivariate test (P = .22). A power analysis indicated that similar studies including a larger cohort would be numerically realistic. These results do not reject the hypothesis that the established epidemiological association between IM and MS results from a stepwise inflammatory propagation from IM sequelae to an MS endophenotype (or presymptomatic trait) in a proportion of IM patients, pending confirmation with adequate power.
Substances chimiques
Biomarkers
0
Cytokines
0
IL1B protein, human
0
Inflammation Mediators
0
Interleukin-1beta
0
Tumor Necrosis Factor-alpha
0
Types de publication
Comparative Study
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
161-168Subventions
Organisme : the European Research Council
ID : 681712
Organisme : Swedish Research Council
ID : 2018-02532
Organisme : Västra Götalandsregionen
ID : FoU 2018
Organisme : Swedish State Support for Clinical Research
ID : ALFGBG-720931
Informations de copyright
© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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