Evidence map›Paper›PMID 30770760›Full record

ArticleArthritis research & therapy2019

Mass spectrometry-based analysis of cerebrospinal fluid from arthritis patients-immune-related candidate proteins affected by TNF blocking treatment.

Johanna Estelius, Johan Lengqvist, Elena Ossipova, Helena Idborg, Erwan Le Maître, Magnus L A Andersson, Lou Brundin, Mohsen Khademi, Elisabet Svenungsson, Per-Johan Jakobsson and 1 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 16 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Johanna EsteliusRheumatology Unit, Department of Medicine, Solna, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Johan LengqvistRheumatology Unit, Department of Medicine, Solna, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Elena OssipovaRheumatology Unit, Department of Medicine, Solna, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Helena IdborgRheumatology Unit, Department of Medicine, Solna, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Erwan Le MaîtreRheumatology Unit, Department of Medicine, Solna, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Magnus L A AnderssonNeuroimmunology Unit, Department of Clinical Neuroscience, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Lou BrundinNeuroimmunology Unit, Department of Clinical Neuroscience, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Mohsen KhademiNeuroimmunology Unit, Department of Clinical Neuroscience, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Elisabet SvenungssonRheumatology Unit, Department of Medicine, Solna, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Per-Johan JakobssonRheumatology Unit, Department of Medicine, Solna, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden.
Jon LampaRheumatology Unit, Department of Medicine, Solna, Center of Molecular Medicine (CMM), Karolinska Institutet, Karolinska University Hospital, SE-17176, Stockholm, Sweden. Jon.lampa@ki.se.
Karolinska Institutet · SEKarolinska University Hospital · SE

Funding

European Union Seventh Framework Programme (FP7/2007-2013) 602919Vetenskapsrådet 2013-9306
6 · The paper itself

Abstract

backgroundSigns of inflammation in cerebrospinal fluid (CSF) of rheumatoid arthritis patients correlate positively with fatigue, a central nervous system (CNS)-related symptom that can be partially suppressed by TNF blockade. This suggests a possible role for CNS inflammation in arthritis that may be affected by TNF blockade. We therefore investigated the effects of TNF blockade on the arthritis CSF proteome and how candidate proteins related to clinical measures of disease activity and inflammation.

methodsMass spectrometry-based quantitative proteomic analysis was performed on CSF from seven polyarthritis patients before and during infliximab treatment. Treatment-associated proteins were identified using univariate (Wilcoxon signed rank test) and multivariate (partial least squares discriminant analysis (PLS-DA)) strategies. Relations between selected candidate proteins and clinical measures were investigated using the Spearman correlations. Additionally, selected proteins were cross-referenced to other studies investigating human CSF in a thorough literature search to ensure feasibility of our results.

resultsUnivariate analysis of arthritis CSF proteome revealed a decrease of 35 proteins, predominantly involved in inflammatory processes, following TNF blockade. Seven candidate proteins, Contactin-1 (CNTN1), fibrinogen gamma chain (FGG), hemopexin (HPX), cell adhesion molecule-3 (CADM3), alpha-1B-glycoprotein (A1BG), complement factor B (CFB), and beta-2-microglobulin (B2M), were selected for further studies based on identification by both univariate and multivariate analyses and reported detection in human CSF and known associations to arthritis. Decreased levels of FGG and CFB in CSF after treatment showed strong correlations with both erythrocyte sedimentation rate and disability scores, while CNTN1 and CADM3 were associated with pain.

conclusionSeveral immune-related proteins in the CSF of arthritis patients decreased during TNF blockade, including FGG and CFB that both correlated strongly with systemic inflammation. Our findings stress that also intrathecal inflammatory pathways are related to arthritis symptoms and may be affected by TNF blockade.

Indexed as

AdultAgedAntirheumatic AgentsArthritis, RheumatoidCell Adhesion MoleculesComplement Factor BFemaleFibrinogenHumansImmunoglobulinsInfliximabMass SpectrometryMiddle AgedProteomeProteomicsTumor Necrosis Factor InhibitorsAntirheumatic AgentsCADM3 protein, humanCell Adhesion MoleculesComplement Factor BFGG protein, humanFibrinogenImmunoglobulinsInfliximabProteomeTumor Necrosis Factor InhibitorsAnkylosing spondylitisAnti-TNFChronic inflammationCSFIntrathecal inflammationJuvenile chronic arthritisProteomicsPsoriatic arthritisRheumatoid arthritis

Identifiers

PMID30770760
PMCPMC6377734
OpenAlexW2912807058

What OpenQuestion holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.