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A neuro-immune model of myalgic encephalomyelitis/chronic fatigue syndrome

Morris, Gerwyn and Maes, Michael 2012, A neuro-immune model of myalgic encephalomyelitis/chronic fatigue syndrome, Metabolic brain disease, pp. 1-18, doi: 10.1007/s11011-012-9324-8.

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Title A neuro-immune model of myalgic encephalomyelitis/chronic fatigue syndrome
Author(s) Morris, Gerwyn
Maes, Michael
Journal name Metabolic brain disease
Start page 1
End page 18
Total pages 18
Publisher Springer New York
Place of publication New York, N. Y.
Publication date 2012-06
ISSN 0885-7490
1573-7365
Keyword(s) chronic fatigue syndrome
inflammation
cytokines
depression
tryptophan
oxidative and nitrosative stress
mitochondria
autoimmune
Summary This paper proposes a neuro-immune model for Myalgic Encephalomyelitis/Chronic fatigue syndrome (ME/CFS). A wide range of immunological and neurological abnormalities have been reported in people suffering from ME/CFS. They include abnormalities in proinflammatory cytokines, raised production of nuclear factor-κB, mitochondrial dysfunctions, autoimmune responses, autonomic disturbances and brain pathology. Raised levels of oxidative and nitrosative stress (O&NS), together with reduced levels of antioxidants are indicative of an immuno-inflammatory pathology. A number of different pathogens have been reported either as triggering or maintaining factors. Our model proposes that initial infection and immune activation caused by a number of possible pathogens leads to a state of chronic peripheral immune activation driven by activated O&NS pathways that lead to progressive damage of self epitopes even when the initial infection has been cleared. Subsequent activation of autoreactive T cells conspiring with O&NS pathways cause further damage and provoke chronic activation of immuno-inflammatory pathways. The subsequent upregulation of proinflammatory compounds may activate microglia via the vagus nerve. Elevated proinflammatory cytokines together with raised O&NS conspire to produce mitochondrial damage. The subsequent ATP deficit together with inflammation and O&NS are responsible for the landmark symptoms of ME/CFS, including post-exertional malaise. Raised levels of O&NS subsequently cause progressive elevation of autoimmune activity facilitated by molecular mimicry, bystander activation or epitope spreading. These processes provoke central nervous system (CNS) activation in an attempt to restore immune homeostatsis. This model proposes that the antagonistic activities of the CNS response to peripheral inflammation, O&NS and chronic immune activation are responsible for the remitting-relapsing nature of ME/CFS. Leads for future research are suggested based on this neuro-immune model.
Language eng
DOI 10.1007/s11011-012-9324-8
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2012, Springer Science+Business Media, LLC
Persistent URL http://hdl.handle.net/10536/DRO/DU:30047548

Document type: Journal Article
Collection: School of Medicine
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Created: Thu, 30 Aug 2012, 09:41:54 EST

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