Journal of IiME Volume 6 Issue 1 (June 2012) from presentations by Dr Vincent Lombardi and Professor Nancy Klimas, it was indisputable that numerous cytokines were significantly different in subjects and controls IL-8 and IL-15 were decreased in patients with ME/CFS, while the pro-inflammatory cytokines (TNF, IL-1, IL-1 and IL-6) and Type 2 cytokines (IL-4, IL-5) were increased in ME/CFS, and the antiinflammatory cytokine IL-13 was reduced: this is consistent with the Th2 or upregulated immune pattern usually seen in ME/CFS Dr Marc Fremont from Belgium showed that bowel dysfunction (dysbiosis, leaky gut, viral infections of the gastric mucosa) is frequently seen in ME/CFS and there is also a Th1/Th2 immune imbalance. Th1 (normal immunity) is antagonistic to the Th17 immune axis. Th17 cells are crucial regulators of inflammation and autoimmunity, and alterations of the Th17 pathway are frequently associated with intestinal disorders such as irritable bowel syndrome. Th17 cells produce IL17F protein and a variant known as His161Arg, which confers protection against inflammation. His161Arg was found in only 6% of people with ME/CFS. This suggests that the Th17 axis and intestinal dysfunction are involved in causing inflammation and possibly in the pathogenesis of ME/CFS The conference confirmed that multiple bodily systems are involved in ME/CFS (this is important, as Wessely School psychiatrists insist that the higher the number of bodily symptoms, the greater the certainty of a somatoform disorder) Possible biomarkers include: salivary HHV6; ATP profiling of ion channel receptors; mitochdondrial energy score; cytokine and chemokine analysis; nearinfrared; EEG profiles; low molecular weight RNase L, and HLA haplotype 4.3.53, MSH, VIP, C4a. Invest in ME (Charity Nr. 1114035) 2009 In “Contemporary Challenges in Autoimmunity”, the Annals of the New York Academy of Sciences published several articles looking at autoimmunity in (ME)CFS. One such paper states: “In association with (ME)CFS physiopathology, immune imbalance, abnormal cytokine profile or cytokine genes, and decreased serum concentrations of complement components have been reported…Many studies have shown the presence of several autoantibodies in (ME)CFS patients. Antibodies to diverse cell nuclear components, phospholipids, neuronal components, neurotransmitters, as well as antibodies against some neurotransmitter receptors of the central nervous system have been described”. The authors consider the different types of antibodies that have been reported in (ME)CFS patients and consider in particular antibodies to nuclear components (52% of (ME)CFS patients are reported as having autoantibodies to components of the nuclear envelope, particularly to lamin B1 molecule); to neurotransmitters and receptors (especially to neurotransmitters such as serotonin (5H-T), adrenals, ACTH and to receptors such as muscarinic cholinergic receptor I and -opioid receptor 1), and to diverse micro-organisms, noting that serum levels of IgA were significantly correlated to the severity of illness. The authors state that the results showed that enterobacteria might be involved in the aetiology of (ME)CFS and that an increased gut-intestinal permeability could cause dysregulation of the immune response to the LPS of gram-negative enterobacteria. The authors note that for many years, enterovirus infection has been associated with (ME)CFS and they note: “However, several negative studies, combined with the rise of the psychiatric ‘biopsychosocial model’ of (ME)CFS have led to a diminished interest in this area” (OD Ortego-Hernandez et al; Ann N Y Acad Sci 2009:1173:600-6009). (For the avoidance of doubt, in the above paper the authors cite only two “negative studies” associated with enteroviral infection in (ME)CFS: the first by Lindh G et al [Scand J Infect Dis www.investinme.org Page 85 of 108
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