Initial results from Bond University academics working to unearth faster diagnosis for CFS

Bond University is undertaking a revolutionary research project aiming to unearth a faster diagnosis method for the debilitating Chronic Fatigue Syndrome (CFS). The researchers are looking for a biomarker for ME/CFS.

The University put out the call for 150 locals aged 20 to 65-years-old to take part in the world-first study, made possible through a $533,000 grant from the Queensland Government’s Smart State program – the first Smart State Grant received by Bond - as well as a $90,000 National Grant from the Mason Foundation to further investigate immunological dysfunction in CFS patients.

Information on the research can be found here.

Initial findings from this research are contained in the following journal article, and are summarised below.

Brenu, E et al (2010) 'Immune and hemorheological changes in Chronic Fatigue Syndrome', Journal of Translational Medicine, vol. 8, no. 1.

Immune and Hemorheological changes in Chronic Fatigue Syndrome

Brenu EW, Staines DR, Baskurt OK, Ashton KJ, Ramos SB, Christy RM, Marshall-Gradisnik SM.

ABSTRACT

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.

PMID: 20064266 [PubMed - as supplied by publisher]