Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Morris, Gerwyn, Maes, Michael, Berk, Michael and Puri, Basant K. 2019, Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?, Metabolic brain disease, vol. 34, no. 2, pp. 385-415, doi: 10.1007/s11011-019-0388-6.

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Title Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?
Author(s) Morris, Gerwyn
Maes, Michael
Berk, MichaelORCID iD for Berk, Michael
Puri, Basant K.
Journal name Metabolic brain disease
Volume number 34
Issue number 2
Start page 385
End page 415
Total pages 31
Publisher Springer
Place of publication New York, N.Y.
Publication date 2019-04
ISSN 0885-7490
Keyword(s) Chronic fatigue syndrome
Endotoxin tolerance
Myalgic encephalomyelitis
Oxidative and nitrosative stress
Summary A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals. The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities. Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation. The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next. Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.
Language eng
DOI 10.1007/s11011-019-0388-6
Field of Research 110999 Neurosciences not elsewhere classified
1103 Clinical Sciences
1109 Neurosciences
Socio Economic Objective 920410 Mental Health
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2019, The Authors
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Document type: Journal Article
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