Journal of IiME Volume 6 Issue 1 (June 2012) the body); four hours later, it was the autonomic genes that showed up. The study that she was presenting in Australia reveals 7 or 8 biomarkers for the illness. (ME)CFS patients should not donate organs; a Holter monitor should be used to look at the heart over a few days -- and a good cardiologist is needed because not all will know about cardiac problems in (ME)CFS. 2010 Following her visit to New Zealand, as one of the world’s leading immunology researchers, in December 2010 Professor Klimas presented her team’s findings at Bond University’s Faculty of Health Sciences and Medicine International Science Symposium on ME/CFS held on 3rd-4th December 2010, Gold Coast, Queensland, Australia, as reported by Dr Rosamund Vallings from New Zealand, extracts from whose summary are reproduced with grateful acknowledgement. Professor Klimas presented a systems biology approach to (ME)CFS. She described (ME)CFS as a disorder of homeostatic imbalance and briefly outlined her 25 year involvement with the disorder, saying she initially worked on the theory that it was a chronic immune activation syndrome, but it was next recognised as a neuroinflammatory disorder, and now genomics have become involved. Repeating some of her presentation in New Zealand (see above), she described an exercise challenge of 8 minutes with measurement of VO2 max, and the evidence that the immunological pathways affected were mainly inflammatory, with the immune cascade leading to many symptoms 4 hours later. Those symptoms involved the endocrine, immune, autonomic and neurological systems. The genes regulating NK cell function which included abnormal perforin and granzyme levels were specifically affected. In this study there was persistent inflammation. There was a huge cascade effect after 8 minutes which persisted 4 hours later. This study confirms that graded exercise is not good for those with (ME)CFS, and patients must stop exercise well short of the aerobic threshold. Other presentations made included that by Hugh Perry, Professor of Experimental Neuropathology, University of Southampton, who discussed how systems behave during inflammation, for example, Invest in ME (Charity Nr. 1114035) “feeling ill”, and how infection leads to an inflammatory response with release of cytokines which then communicate with the brain, leading to malaise; he noted that systemic inflammation activates selective brain regions, a mechanism that works through macrophages in the brain via the blood-brain barrier. Professor Mary Ann Fletcher (University of Miami) presented her work on biomarkers for (ME)CFS, initially looking at NK cell function and the diminution of perforin and granzyme, then at neuropeptide Y , which is involved in the stress reaction and she showed how, in a controlled study, NPY was considerably higher in (ME)CFS compared with controls and how ROC analysis showed discrimination between (ME)CFS patients and controls, where NPY was found to be 80% sensitive in (ME)CFS. NYP also correlates with disease severity in (ME)CFS. Ekua Brenu (PhD candidate, Bond University, Queensland, Australia, under the direction of Professor Sonya Marshall-Gradisnik, one of Australia’s foremost researchers in neuroimmunology) had looked at innate and adaptive immunity in (ME)CFS seeking biomarkers in a study of 253 patients and 100 controls at baseline and at 6 months. Cytotoxic activity of NK cells and CD8+T cells was significantly reduced, and perforin and granzyme activity was reduced. When looking at NK cell phenotypes, CD56 bright cells were significantly diminished. Cytokine secretion from CD+4 T cells showed significant elevation of IL-10, IFN and TNF; FOXP3 expression was also heightened in the (ME)CFS group. Vaso-active intestinal peptide (VIP, an endoegenous and exogenous immunomodulator) receptors were also investigated and found to be significantly elevated. Donald Staines (Bond University, Gold Coast, Australia; Associate Professor and Public Health Physician at PHANU – Australia’s Public Health and Neuroimmunology Unit), considered whether autoimmunity affecting vaso-active neuropeptides suggest a pathomechanism for (ME)CFS, as (ME)CFS may be associated with autoimmunity affecting the function of vaso-active neuropeptides such as VIP and PACAP (pituitary adenylate cyclase activating peptide); VIP/PACAP synergism is involved with potentiation of cardiac www.investinme.org Page 90 of 108
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