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Published in: Metabolic Brain Disease 2/2019

Open Access 01-04-2019 | Fatigue | Review Article

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

Authors: Gerwyn Morris, Michael Maes, Michael Berk, Basant K. Puri

Published in: Metabolic Brain Disease | Issue 2/2019

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Abstract

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.
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Metadata
Title
Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?
Authors
Gerwyn Morris
Michael Maes
Michael Berk
Basant K. Puri
Publication date
01-04-2019
Publisher
Springer US
Keyword
Fatigue
Published in
Metabolic Brain Disease / Issue 2/2019
Print ISSN: 0885-7490
Electronic ISSN: 1573-7365
DOI
https://doi.org/10.1007/s11011-019-0388-6

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