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Proteomic Signatures in Cerebrospinal Fluid and Their Clinical Associations in Patients with ME/CFS

ABSTRACT: This study evaluated the cerebrospinal fluid (CSF) proteomes from 31 patients diagnosed with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). We quantified 902 proteins, each expressed in at least eleven samples, and systematically categorized clinical factors relevant to ME/CFS symptoms—including autonomic dysfunction, neuroinflammation and metabolic disturbances.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cerebrospinal Fluid

DISEASE(S): Chronic Fatigue Syndrome

SUBMITTER: Peng Li

LAB HEAD: Jonas Bergquist

PROVIDER: PXD076216 | Pride | 2026-04-06

REPOSITORIES: Pride

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			Action	DRS
	P01_severe_POTS.raw	Raw
	P02_severe_NoPOTS.raw	Raw
	P03_moderate_NoPOTS.raw	Raw
	P04_moderate_POTS.raw	Raw
	P05_moderate_NoPOTS.raw	Raw

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Publications

Proteomic signatures in cerebrospinal fluid and their clinical associations in patients with ME/CFS.

Bragée Björn B Li Peng P Meadows Danielle D Widgren Anna A Sjögren Per P Ghatan Per Hamid PH Bertilson Bo C BC Xiao Wenzhong W Bergquist Jonas J

Scientific reports 20260403

This study evaluated the cerebrospinal fluid (CSF) proteomes from 31 patients diagnosed with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). We quantified 902 proteins, each expressed in at least eleven samples, and systematically categorized clinical factors relevant to ME/CFS symptoms-including autonomic dysfunction, neuroinflammation and metabolic disturbances. Differentially expressed protein and pathway analyses evaluated protein features associated with both postural orthostat ...[more]

PMID: 41932997

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Extracellular vesicle protein and miRNA signatures as biomarkers for post-infectious ME/CFS patients

Project description:Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic disease with a yet unresolved pathophysiology and sparse diagnostic options. Extracellular vesicles (EVs) serve as carriers of disease-specific protein and microRNA (miRNA) signatures. We aim to identify novel miRNA markers as potential biomarker in isolated plasma EVs from female post-COVID-19 ME/CFS patients in comparison to healthy controls (HCs). EVs were isolated from plasma of post-infectious ME/CFS patients and HCs by size exclusion chromatography, and characterized for their number, size, morphology and surface marker expression. Small RNA sequencing identifed four small RNAs, which are significantly differential expressed between ME/CFS patients and healthy donors. Subsequently performed qPCR studies revealed significant downregulation exclusively for the hsa-let-7b-5p miRNA in EVs from ME/CFS patients versus HCs. Notably, reduced hsa-let-7b-5p expression correlated with impaired physical functioning as well as increased fatigue, pain, and immune activation scores. Our data indicate, that hsa-let-7b-5p could serve as a promising candidate for development as diagnostic and stratification marker of ME/CFS.

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Metabolomics Workbench ST000910 - GNPS - Insights into the pathogenesis of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) through metabolomic profiling of cerebrospinal fluid (part I)

Project description:Insights into the pathogenesis of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) through metabolomic profiling of cerebrospinal fluid

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Whole blood human transcriptome and virome analysis of ME/CFS patients experiencing post-exertional malaise following cardiopulmonary exercise testing

Project description:Myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) is a syndrome of unknown etiology characterized by profound fatigue exacerbated by physical activity, also known as post-exertional malaise (PEM). Previously, we did not detect evidence of immune dysregulation or virus reactivation outside of PEM periods. Here we sought to determine whether cardiopulmonary exercise stress testing of ME/CFS patients could trigger such changes. ME/CFS patients (n=14) and matched sedentary controls (n=11) were subjected to cardiopulmonary exercise on 2 consecutive days and followed up to 7 days post-exercise, and longitudinal whole blood samples analyzed by RNA-seq. Although ME/CFS patients showed significant worsening of symptoms following exercise versus controls, with 8 of 14 ME/CFS patients showing oxygen consumption (V̇O2) on day 2, transcriptome analysis yielded only 6 differentially expressed gene (DEG) candidates when comparing ME/CFS patients to controls across all time points. None of the DEGs were related to immune signaling, and no DEGs were found in ME/CFS patients before and after exercise. Virome composition (P=0.746 by chi-square test) and number of viral reads (P = 0.098 by paired t-test) were not significantly associated with PEM. These observations do not support transcriptionally-mediated immune cell dysregulation or viral reactivation in ME/CFS patients during symptomatic PEM episodes.

2019-03-09 | GSE128078 | GEO

Transcriptome analysis of circulating monocytes in QFS and CFS compared to various control groups

Project description:Transcriptomes of circulating monocytes in Q fever fatigue syndrome (QFS) patients, chronic fatigue syndrome (CFS) patients, asymptomatic Q fever seropositive controls and healthy controls

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Mapping the complexity of ME/CFS: Evidence for abnormal energy metabolism, altered immune profile and vascular dysfunction

Project description:Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex disorder with no known underlying mechanisms, diagnostic tools, or treatments. Multiple areas of dysfunction have been extensively studied, but rarely examined together. We recruited age- and sex-matched ME/CFS patients and healthy controls for a multi-modal study examining energy metabolism, immune profiles and plasma protein levels. Adenosine monophosphate (AMP) were higher in immune cells from MECFS patients, with a similar but non-signficant trend observed in plasma. Additionally, immune cells showed higher levels of adenosine diphosphate (ADP) and a reduced adenosine triphosphate/adenosine diphosphate (ATP/ADP) ratio. These findings imply decreased ATP generation and the presence of energy stress within the immune cell population. Adaptive immune cell populations were skewed towards less mature effector subsets of CD4+, CD8+ and γδ T cells, and proportions of CD1c+CD141- conventional DC type 2 (cDC2) and CD56lowCD16+ terminal natural killer (NK) cells were also reduced. Elevated levels of plasma proteins associated with thrombus formation and vascular reactivity may contribute to the endothelial dysfunction observed in ME/CFS patients. Using Classification and Regression Tree (CART) modelling, we identified variables from each mode of investigation with strong predictive potential for ME/CFS. Together, this study provides new insights intothe somatic symptoms and underlying biology of ME/CFS.

2025-11-14 | PXD068504 | Pride

Deep phenotyping of Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome [Protein]

Project description:Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling disorder that may occur following an infection, yet the clinical phenotype is poorly defined, the pathophysiology is unknown, and no disease-modifying treatments are available. We used rigorous criteria to recruit a cohort of post-infectious ME/CFS (PI-ME/CFS) volunteers (n=17) with matched healthy controls (n=21) to conduct deep clinical and biological phenotyping using an extensive battery of tests. Among the many physical and cognitive complaints, one defining feature of PI-ME/CFS was an alteration of effort preference, rather than physical or central fatigue, due to dysfunction of integrative brain regions potentially associated with central catechol pathway dysregulation, with consequences on autonomic functioning and physical deconditioning. Immune profiling suggested chronic antigenic stimulation with increase in naïve and decrease in switched memory B-cells. Alterations in gene expression profiles of peripheral blood mononuclear cells and metabolic pathways were consistent with cellular phenotypic studies and demonstrated differences according to sex. Together these clinical abnormalities and biomarker differences provide unique insight into the underlying pathophysiology of PI-ME/CFS, which may guide future intervention.

2023-12-22 | GSE251790 | GEO

Deep phenotyping of Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome [PBMC RNA-Seq]

2023-12-22 | GSE251872 | GEO

Deep phenotyping of Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome [Protein plasma]

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Deep phenotyping of Post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome [RNA-Seq]

2023-10-31 | GSE245661 | GEO

Passive transfer of IgG immune complex from ME/CFS patients alters mitochondrial architecture and function

Project description:Autoimmunity is an established clinical feature in both Myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) and Post-Acute Sequelae of COVID (PASC). Passive transfer of immunoglobulins from patients' sera into mice induces some clinical features of PASC. IgG-induced transfer of disease phenotypes has long been appreciated, yet the exact mechanism of disease development remains largely elusive. Here, we show that IgG isolated from ME/CFS patients selectively induces mitochondrial fragmentation in primary human endothelial cells and alters mitochondrial energetics. Blocking IgG entry into cells using an Fc blocker inhibits the mitochondrial fragmentation phenotype. Both the digested Fab and Fc regions of IgG separately entered the endothelial cells. However, only the Fab fragment alone was able to alter the mitochondrial energetics, similar to native IgG. Proteomics analysis of IgG-bound immune complex revealed significant and specific changes within the immune complex of ME/CFS and PASC patients compared to healthy controls and other disease controls. We demonstrate that IgGs from ME/CFS patients carry a chronic protective response signal that promotes mitochondrial adaptation to stress through mitochondrial fragmentation, without altering mitochondrial ATP generation capacity in endothelial cells. Our results suggest that chronic and pathogenic IgG-induced mitophagy and metabolic alterations to stress-dependent ATP production may lead to cellular saturation, ultimately affecting mitochondrial health. These results provide an opportunity to develop alternative therapeutic intervention strategies.

2026-02-23 | PXD065439 | Pride

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