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2008 - Evidence of inflammatory immune signaling in CFS: gene expression in peripheral blood

Discussion in 'Latest ME/CFS Research' started by Bob, Aug 12, 2015.

  1. Bob

    Bob

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    Open access.

    This isn't new but I can't find a dedicated discussion about it on the forum, so I thought I'd post it. It's a paper from 2008 that explores abnormalities in gene expression in immune cells including B cells. (Note that it uses the empirical definition - so it may be a heterogeneous cohort of people who experience fatigue.)

    I've only just come across it so I haven't yet read the full paper, but the abstract is eye-catching, especially the conclusion.


    Evidence of inflammatory immune signaling in chronic fatigue syndrome: A pilot study of gene expression in peripheral blood.
    Aspler AL, Bolshin C, Vernon SD, Broderick G.
    2008 Sep 26.
    Behav Brain Funct. 4:44.
    doi: 10.1186/1744-9081-4-44.
    http://www.ncbi.nlm.nih.gov/pubmed/18822143

    Full paper:
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2569951/
    http://www.behavioralandbrainfunctions.com/content/4/1/44

     
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  2. Bob

    Bob

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    @Jonathan Edwards, perhaps you might be interested in this paper, if you haven't already seen it? It also includes a range of interesting references relating to research of immune-cells in ME patients.
     
    Last edited: Aug 12, 2015
  3. Jonathan Edwards

    Jonathan Edwards "Gibberish"

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    Thanks Bob,
    I am not overimpressed by what is in the abstract but will try to look at the full paper. A difficulty with looking at gene expression in circulating B cells is that you are grouping together cells at very different stages of maturation and differentiation. A slight shift in trafficking will alter proportions of cells with quite different activities.
     
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  4. Marco

    Marco Grrrrrrr!

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    Fair point - if you're comparing one individual to another but with sample sizes of approx 70 'fatigue patients' and 35 controls - wouldn't the 'slight shift in trafficking' even out? (just a technical question - I'm not convinced there's anything meaningful here).
     
  5. anciendaze

    anciendaze Senior Member

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    There is a fundamental problem here because this cohort was put together using the Reeves "empirical" definition. It could well be dominated by patients with major depressive disorders.

    I do think there is evidence of inflammatory processes both in many cases of depression and in ME/CFS. What would be very interesting would be to test for levels of PEPITEM or active genes producing it, to see if there was a defect in the signalling to limit recruitment of cytotoxic T-cells to endothelial tissues. Inflammation in capillaries by such a runaway process would be essentially invisible in ordinary clinical examination.

    Unfortunately, this research didn't take place at a time when PEPITEM signalling was known.
     
  6. Jonathan Edwards

    Jonathan Edwards "Gibberish"

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    I agree that if the statistics are good there would still seem to be a difference of some sort. My worry is that it is interpreted as a difference in function of a cell type when it may simply be a shift in trafficking. Both might be interesting but the interpretation in terms of an inflammatory process or whatever might be premature. When we study B cells we essentially do not bother to look at the whole CD19 population because it is too heterogeneous and any changes are impossible to interpret. I tend to worry when people talk of shifts in gene expression without breaking it down into specific cell types.
     
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