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Immune and hemorheological changes in Chronic Fatigue Syndrome

Discussion in 'Latest ME/CFS Research' started by DysautonomiaXMRV, Jan 12, 2010.

  1. 'Immune and hemorheological changes in Chronic Fatigue Syndrome'

    Ekua Brenu, Donald Staines, Oguz Baskurt, Kevin Ashton, Sandra Ramos,
    Rhys Christy, Sonya Marshall-Gradisnik
    Journal of Translational Medicine 2010, 8:1


    Chronic Fatigue Syndrome (CFS) is a multifactorial disorder that
    affects various physiological systems including immune and
    neurological systems. The immune system has been substantially
    examined in CFS with equivocal results, however, little is known about
    the role of neutrophils and natural killer (NK) phenotypes in the
    pathomechanism of this disorder. Additionally, the role of erythrocyte
    rheological characteristics in CFS has not been fully expounded. The
    objective of this present study was to determine deficiencies in
    lymphocyte function and erythrocyte rheology in CFS patients.


    Flow cytometric measurements were performed for neutrophil function,
    lymphocyte numbers, NK phenotypes (CD56dimCD16+ and CD56brightCD16-)
    and NK cytotoxic activity. Erythrocyte aggregation, deformability and
    fibrinogen levels were also assessed.


    CFS patients (n = 10) had significant decreases in neutrophil
    respiratory burst, NK cytotoxic activity and CD56brightCD16- NK
    phenotypes in comparison to healthy controls (n = 10). However,
    hemorheological characteristics, aggregation, deformability and
    fibrinogen, lymphocyte numbers and CD56dimCD16+ NK cells were similar
    between groups.


    Immune dysfunction may therefore be an important contributory factor
    to the mechanism of CFS, as indicated by decreases in neutrophil
    respiratory burst, NK cell activity and NK phenotypes. Thus, immune
    cell function and phenotypes are possible diagnostic markers for CFS.
  2. kurt

    kurt Senior Member

    That is a great study, thanks for the link, good reading.

    What caught my attention was that the cytotoxicity of the NK cells was approximately one third of normal. That is huge and means our NK cells are simply too weak to kill all but the weakest viruses. So of course we have higher viral load.

    Here is the result of the cytotoxic study:

    All I can say is WOW, this is a smoking gun for CFIDS. So in CFS our NK cells are only about 40% as deadly in their attacks on pathogens as normal NK cells (13.6%/34.3%=39.7%).

    From the conclusion of the paper:

    If CFS were funded normally as a regular disease should be, this study would be quickly replicated with a larger 'N' (this was only N=10). So PWC appear to have an altered adaptive immune response.
  3. fresh_eyes

    fresh_eyes happy to be here

    mountains of north carolina
    Kurt, thanks so much for putting this in terms I can understand! Wow indeed.
  4. Athene

    Athene ihateticks.me

    Kenny De Meirleir did these tests on me - as far as I know he does on all his patients. My results were like those described in the paper. I think he must have a vast amount of patient data on this. I find it hard to find his research online but I wonder if he has published anything on this?

    BTW dysautonomia, thank you for all your posts. You constantly bring up very interesting and informative topics and I really appreciate your contribution here.
  5. fairlight



    I think that CFS is an immune disorder that we are predisposed to and wil have to be treated as a disease of the immune system. This is why people have had good results with rituxan, methotrexate and stem cell transpalnts. I don't think anti-virals are the answer for many of the cases . (Just my opinion).

    Thanks for posting this study.
  6. Countrygirl

    Countrygirl Senior Member

  7. Gerwyn

    Gerwyn Guest

    With the HPA axis depressed,as found in many studies,the immune system is permanently switched on to a lesser or greater degree----I know i did,t catch anything for years now I,m better I catch practically everything.Dr Myhill provides a better and more detailed explanation than me.
  8. Countrygirl

    Countrygirl Senior Member

    Thank you Gerwyn. I'm still puzzled though. Does it mean that our feeble, much-reduced NK cells are just being flogged to death ? They must be knackered!

    So it sounds like a chicken-and-egg scenario here: which came first - the virus or the depression of the HPA ?

    Can someone remind me, if we ever knew, how XMRV can cause the HPA dysfunction?


    Brain dead.
  9. Hi Countrygirl,

    I was under the impression that some cold symptoms are actually by-products of your body responding to the virus. Runny nose for example - that's your body kicking out the dead virus bits being swept up from your throat and lungs, right? (Spoken like a true non-scientist.) So if your body were unable to fight a cold it would just contribute to your general feeling of ill-health rather than manifesting itself as a true cold. But I could be completely wrong about that -- somebody please enlighten me!

    I'd be wary of relying on anecdotal evidence as supporting / not supporting any theory. If there's a research paper which investigates whether M.E. patients catch colds less frequently, I'd be very interested to see it. I have caught a cold since contracting M.E. and it completely undid my recovery - I was bed-bound again. However, before my second relapse on October last year, I seldom caught colds.

    Rachel xx
  10. Dolphin

    Dolphin Senior Member

    I just read this and found it interesting.

    Note: I think the references go off somewhere around 12/13 and that [x] refers to x+1 in the references for a lot of the paper. I have just written to the corresponding author to tell them.

    Looking at Figure 4, it is surprising that there is no statistically significant difference between them. I think a larger sample might have found a difference.
    This is to do with Les Simpson's work. I had an abnormal test with him before (I would need to check it to see which type).
  11. Dolphin

    Dolphin Senior Member

    Here's what I wrote to them in case anyone is wondering:

    They said they were going to fix it but 2.5 years later, it hasn't been done. Not the end of the world of course.

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