Evidence map›Paper›PMID 20447453›Full record

ArticleBrain, behavior, and immunity2010

A formal analysis of cytokine networks in chronic fatigue syndrome.

Gordon Broderick, Jim Fuite, Andrea Kreitz, Suzanne D Vernon, Nancy Klimas, Mary Ann Fletcher

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 3 pooled it
9.8field-weighted citation impact, top 1% 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

117 citing papers in PubMed, 3 syntheses or guidelines pooled it, 208 citations in OpenAlex.

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57 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 2 countries.

Gordon BroderickDivision of Pulmonary Medicine, Department of Medicine, University of Alberta, College Plaza, 8215 112 Street NW, Edmonton, Alberta, Canada. gordon.broderick@ualberta.ca
Jim Fuite
Andrea Kreitz
Suzanne D Vernon
Nancy Klimas
Mary Ann Fletcher
University of Alberta · CASolve ME/CFS Initiative · USUniversity of Miami · USVeterans Health Administration · US

Funding

Immunologic Mechanisms, Biomarkers and Subsets in Chronic Fatigue Syndrome (CFS)R01AI065723 · NIAID · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FLETCHER, MARY A · 2007 to 2011
$1.9M
Neuropeptide Y and dipeptidyl-peptidase IV (CD26) in chronic fatigue syndromeR21AA016636 · NIAAA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FLETCHER, MARY A · 2006 to 2007
$395k
NIAAA NIH HHS R21AA016635NIAAA NIH HHS R21 AA016636NIAID NIH HHS R01 AI065723NIAID NIH HHS R01AI065723
6 · The paper itself

Abstract

Chronic Fatigue Syndrome (CFS) is a complex illness affecting 4 million Americans for which no characteristic lesion has been identified. Instead of searching for a deficiency in any single marker, we propose that CFS is associated with a profound imbalance in the regulation of immune function forcing a departure from standard pre-programmed responses. To identify these imbalances we apply network analysis to the co-expression of 16 cytokines in CFS subjects and healthy controls. Concentrations of IL-1a, 1b, 2, 4, 5, 6, 8, 10, 12, 13, 15, 17 and 23, IFN-γ, lymphotoxin-α (LT-α) and TNF-α were measured in the plasma of 40 female CFS and 59 case-matched controls. Cytokine co-expression networks were constructed from the pair-wise mutual information (MI) patterns found within each subject group. These networks differed in topology significantly more than expected by chance with the CFS network being more hub-like in design. Analysis of local modularity isolated statistically distinct cytokine communities recognizable as pre-programmed immune functional components. These showed highly attenuated Th1 and Th17 immune responses in CFS. High Th2 marker expression but weak interaction patterns pointed to an established Th2 inflammatory milieu. Similarly, altered associations in CFS provided indirect evidence of diminished NK cell responsiveness to IL-12 and LT-α stimulus. These observations are consistent with several processes active in latent viral infection and would not have been uncovered by assessing marker expression alone. Furthermore this analysis identifies key sub-networks such as IL-2:IFN-γ:TNF-α that might be targeted in restoring normal immune function.

Indexed as

Models, ImmunologicalAdultBiomarkersCase-Control StudiesCytokinesFatigue Syndrome, ChronicFemaleHumansInterferon-gammaInterleukinsKiller Cells, NaturalLymphotoxin-alphaMiddle AgedSignal TransductionTh17 CellsTh1 CellsBiomarkersCytokinesInterferon-gammaInterleukinsLymphotoxin-alphaTumor Necrosis Factor-alpha

Identifiers

PMID20447453
PMCPMC2939140
OpenAlexW1981982266

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.