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A Formal Analysis of Cytokine Networks in Chronic Fatigue Syndrome

Discussion in 'Latest ME/CFS Research' started by shrewsbury, May 9, 2010.

  1. shrewsbury

    shrewsbury member

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    Broderick G, Fuite J, Kreitz A, Vernon SD, Klimas N, Fletcher MA.
    Brain Behav Immun. 2010 May 3. [Epub ahead of print]

    Department of Medicine, University of Alberta, Edmonton, Alberta, Canada.

    http://www.ncbi.nlm.nih.gov/pubmed/20447453

    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
    preprogrammed 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-gamma, lymphotoxin-alpha (LT-alpha) and
    TNF-alpha 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
    esponses in CFS. High Th2 marker expression but weak interaction
    atterns pointed to an established Th2 inflammatory milieu.

    Similarly, altered associations in CFS provided
    indirect evidence of diminished NK cell responsiveness to IL-12 and
    LTalpha 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:IFNgamma:TNFalpha
    that might be targeted in restoring normal immune function.

    Copyright 2010. Published by Elsevier Inc.

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