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

Morris, Gerwyn; Maes, Michael

doi:10.1007/s11011-012-9324-8

Cited by 117Fibromyalgia and Chronic Fatigue Syndrome ResearchLong-Term Effects of COVID-19Tryptophan and brain disorders

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

Morris, Gerwyn, Maes, Michael·2013·Metabolic Brain Disease

DOI 10.1007/s11011-012-9324-8

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Abstract

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.

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HPG dysregulation may increase blood-brain barrier permeability, allowing infiltration of immune cells into the brain to establish or sustain a low-grade neuroinflammatory profile.
“Thus, HPG dysregulation may increase blood-brain barrier permeability, allowing infiltration of immune cells into the brain to establish or sustain a low-grade neuroinflammatory profile as put forward by Morris and Maes17.”
From Leveraging Prior Knowledge of Endocrine Immune Regulation in the Therapeutically-relevant Phenotyping of Women with Chronic Fatigue Syndrome (2019) · cites this paper as [17]

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Authors: Morris, G., & Maes, M.
Affiliations: Piyavate Hospital (TH)
Corresponding author: Maes, Michael
ORCID: Morris, Gerwyn
Maes, Michael
Venue: Metabolic Brain Disease
Publisher: Springer Science and Business Media LLC
Published: 2012-06-21
Volume: 28
Issue: 4
Pages: 523-540
ISSN: 0885-7490 (ISSN-L)
1573-7365
DOI: 10.1007/s11011-012-9324-8
OpenAlex: W2035315327
Cited by: 117
References: 207
Citations by year: 2026: 5 · 2025: 5 · 2024: 9 · 2023: 6 · 2022: 8 · 2021: 7 · 2020: 1 · 2019: 11 · 2018: 7 · 2017: 5 · 2016: 14 · 2015: 16 · 2014: 9 · 2013: 14
FWCI: 1.68
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Metabolic Brain Disease (publishedVersion)
PubMed (publishedVersion)
Funders: World Health Organization
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords: chronic fatigue syndrome, inflammatory cytokines, NF-κB, mitochondrial dysfunction, autoreactive T cells, autoimmunity, molecular mimicry, bystander activation, epitope spreading, microglial activation, vagus nerve, post-exertional malaise, immune activation
MeSH terms: Brain, Fatigue, Humans, Inflammation, Models, Biological, Fatigue Syndrome, Chronic, Cytokines, Oxidative Stress

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

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