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Latest Research in Immunology
The immunological profile of an Australian CFS female population was presented by Ekua Brenu (Gold Coast, Australia). She noted a 0.2% prevalence of CFS is Australia, with $A59 million per annum spent in the management of CFS. Blood samples were taken from 8 CFS patients and 8 controls. Neutrophil function was studied with respect to respiratory burst and phagocytic activity. CFS patients demonstrated significant decrease in respiratory burst, but increased phagocytic activity did not attain significance. T cells, B cells and monocytes were observed in patients and controls.
Christopher Snell (Stockton, USA) did not find that either RNaseL ratio or elastase have any efficacy as biomarkers for CFS. There was high variability for both measures in CFS and controls, and these levels may be influenced by factors other than illness. RNaseL activity may not be unique to CFS.
Gordon Broderick (Edmonton, Canada) found that subjects with Gulf War Illness (GWI) can be discriminated by demonstrating significantly different neuro-endocrine-immune dynamics in response to exercise. Changes in cytokines, NPY and cortisol are evident both at rest and much more so under challenge, and could separate subjects completely from the control group.
Subgrouping of CFS patients was addressed by Vincent Lombardi (Reno, USA) looking at cytokine and chemokine profiles. He used microarray, a Random Forest computational program, to delineate CFS patients from healthy controls. Each subgroup was found to display a unique cytokine/chemokine signature. This has potential to subgroup patients using serum biomarkers in an approach to appropriate treatments. (Anti-inflammatory, antiviral or antimicrobial).
Nancy Klimas (Miami, USA) has found that cytokine abnormalities are common in CFS, with potential as biomarkers or targets for treatment strategies. Cost effectiveness with newer techniques should make these tests more readily available to evaluate a large panel of cytokines. The study presented demonstrated a disorganized pattern of the cytokines regulating Th1 dependent lymphocyte function, critical to antiviral defense. The data supports a Th2 shift, pro-inflammatory cytokine cascade activation and down regulation of components of cytotoxic cell function.
Nicole Porter (Chicago, USA) showed the importance of looking at viral versus non-viral onset in CFS, with differences in cytokine production and expression. In the viral group there was Th1 shift and in the non-viral group a Th2 shift. Viral and bacterial onset patients should be separated in future studies. A pattern of protein production in the non-viral group is likely to be immune cell mediated anti-inflammatory activity with chronic suppression of immune system activation. In the viral group, there is pro-inflammatory activation with persistent hyper-immune response.