Journal of IiMER Volume 10 Issue 1 June 2016 IIMEC11 PRESENTERS Biological markers (biomarkers) are objective measures of biological phenomena. Among possible biomarkers are the physical appearance of an organism or its components, amounts of molecules or cell types, responses of cells or tissue to a stimulus, enzyme activities, gene sequences, or level of interactions of one molecules with another. Many potential biomarkers for the identification of victims of ME/CFS have been measured in the past in the hope of understanding the pathophysiology of the disease. Such studies have revealed abnormalities in function, population and gene expression in immune cells, disturbances in brain morphology and operation, abnormal gas exchange parameters in exercise physiology, discordant levels of plasma signaling proteins, and atypical autonomic function. While these abnormalities have provided some hints about the biological basis of the disease, much more information is needed to understand its underlying cause. Furthermore, the existing biomarkers are cumbersome to implement in a medical office setting, not available to be performed typical medical testing labs, and are not able to identify all patients that can be diagnosed with the disease by an experienced ME/CFS physician. We explored the possibility that levels of inflammatory proteins in the blood, in conjunction with bacterial species abundance in the gut microbiome, might serve as biomarkers for diagnosis if the intestinal microbiome is disturbed in ME/CFS. We examined the bacterial microbiome in 48 ME/CFS patients in 39 healthy controls by sequencing regions of DNA that allow identification of the different types of bacteria that are present. We found that ME/CFS patients had reduced diversity in bacterial types in comparison to healthy individuals, a finding that has also been reported in Crohn’s disease and ulcerative colitis. While there is no set of species detected that is present in ME/CFS patients that is absent from healthy individuals, we identified a number of taxonomic groups that were represented in different abundance between ME/CFS patients and controls. By applying a statistical method to the blood analyses and the bacterial compositions, we were able to classify 83% of the subjects correctly as either patients or healthy individuals. Our results are consistent with an ongoing damage to the gut that leads to greater microbial translocation into the blood, which could then have adverse effects on the immune system. The difference in population structure of the microbial community may be contributing to some ME/CFS symptoms and to their severity. However, there is no evidence that the disturbance in the gut microbiome is a cause of the disease rather than being one of its symptoms. Invest in ME (Charity Nr. 1114035) www.investinme.org Page 69 of 77
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