Journal of IiME Volume 8 Issue 1 later Associate Professor. He joined University of Leeds as Professor of Molecular Immunology in the Institute of Molecular and Cellular Biology in 1999. His scientific interests are in understanding how the immune response in the gut functions and in particular, is able to distinguish between the commensal microbes that reside in the gut and environmental microbes that cause disease, and in the mechanisms by which the body's immune system no longer ignores or tolerates commensal gut bacteria and how this leads to immune system activation and inflammatory bowel disease. #IIMEC9 Abstract: A role for a leaky gut and the intestinal microbiota in the pathophysiology of myalgia encephalomyelitis/ chronic fatigue syndrome? Simon R Carding1,2, Tom Wileman1, Daniel Vipond1,2, Bharat Harbham1, Eleanor Cottam3 and Amolak Bansal4 1Norwich Medical School, University of East Anglia, 2Gut Health and Food Safety Research Programme, Institute of Food Research, Norwich Research Park, Norwich, 3The Pirbright Institute, Woking, 4Dept. Immunology, St. Helier NHS Trust, Carshalton. Recent studies point to a link between autoimmunity and myalgic encephalomyelitis (ME) raising the possibility that the neuro-inflammation seen during ME may be triggered by systemic infections. The gastrointestinal tract contains a vast population of resident microbes (the microbiota) consisting primarily of bacteria and fungi, yeasts and viruses. The microbiota influences intestinal barrier function and host defences against microbial challenge with microbial dysbiosis leading to both local and systemic chronic inflammation. The microbiota may also influence cognitive function and behaviour. It is known that gut infections can cause anxiety, depression and cognitive dysfunction; and microbefree, germfree mice that have no intestinal microbiota display alterations in stress-responsivity, central neurochemistry and behaviour indicative of a reduction in anxiety. Many ME patients have gastrointestinal disturbance, are more likely to develop irritable bowel syndrome, and may have increased intestinal permeability (a “leaky” gut”). Together these observations suggest that changes in intestinal barrier integrity, which may be driven May 2014 by or are a consequence of intestinal dysbiosis, as a result, for example, of a gut infection could contribute to ME by driving systemic inflammation and/or influencing the microbiota-gut-brain axis. With support from Invest in ME we have initiated a project to address the hypothesis that alterations in intestinal barrier integrity and the resulting influx of luminal antigens triggers and perpetuates a state of chronic inflammation both locally and systemically that contributes to the pathophysiology of CFS/ME. The aim of this three-year, multi-centre collaborative project therefore is to determine if alterations in the intestinal barrier integrity and microbiota composition and function exist in CFS patients. Professor Sonya MarshallGradisnik School of Medical Sciences, Griffith University, Australia Professor Marshall-Gradisnik is one of Australia's foremost researchers in the area of neuroimmunology and has been instrumental in establishing the Public Health and Neuroimmunology Unit (PHANU) at Bond University, and now at Griffith University. Much of her work relates specifically to autoimmunity in Chronic Fatigue Syndrome sufferers and she is regularly asked to speak to community groups on behalf of Queensland Health and NSW Health. Her research in the area of exercise immunology has also contributed to the body of knowledge relating to the effect of doping in sport and she serves as Sports Medicine Australia's national spokesperson in this area. The vital research conducted by Professor Marshall has attracted more than $1 million in grant funding Invest in ME (Charity Nr. 1114035) www.investinme.org Page 43 of 52

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