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Immune cell function and phenotypes are possible diagnostic markers for CFS

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

  1. Daisymay

    Daisymay Senior Member

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    Interesting research on natural killer cell function, though they are loking at very small numbers of patients so far.

    "decreases in neutrophil respiratory burst" - wonder if this fitsa in with Dr Myhill's paper on reduced mitochondrial functioning?

    BW,

    Daisymay


    http://www.translational-medicine.com/content/8/1/1

    Immune and hemorheological changes in Chronic Fatigue Syndrome

    Ekua W Brenu email, Donald R Staines email, Oguz K Baskurt email, Kevin J Ashton email, Sandra B Ramos email, Rhys M Christy email and Sonya M Marshall-Gradisnik email

    Journal of Translational Medicine 2010, 8:1doi:10.1186/1479-5876-8-1
    Published: 11 January 2010
    Abstract (provisional)

    Background

    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.
    Methods

    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.
    Results

    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.
    Conclusion

    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.

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