Metabolic Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Not Due to Anti-mitochondrial Antibodies.

AMA PDC anti-mitochondrial autoantibodies anti-pyruvate dehydrogenase complex antibodies myalgic encephalomyelitis/chronic fatigue syndrome

Journal

Frontiers in medicine
ISSN: 2296-858X
Titre abrégé: Front Med (Lausanne)
Pays: Switzerland
ID NLM: 101648047

Informations de publication

Date de publication:
2020
Historique:
received: 18 10 2019
accepted: 10 03 2020
entrez: 17 4 2020
pubmed: 17 4 2020
medline: 17 4 2020
Statut: epublish

Résumé

Metabolic profiling studies have recently indicated dysfunctional mitochondria in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This includes an impaired function of pyruvate dehydrogenase complex (PDC), possibly driven by serum factor(s), which leads to inadequate adenosine triphosphate generation and excessive lactate accumulation. A reminiscent energy blockade is likely to occur in primary biliary cholangitis (PBC), caused by anti-PDC autoantibodies, as recently proposed. PBC is associated with fatigue and post-exertional malaise, also signifying ME/CFS. We herein have investigated whether ME/CFS patients have autoreactive antibodies that could interfere with mitochondrial function. We found that only 1 of 161 examined ME/CFS patients was positive for anti-PDC, while all PBC patients (15/15) presented significant IgM, IgG, and IgA anti-PDC reactivity, as previously shown. None of fibromyalgia patients (0/14), multiple sclerosis patients (0/29), and healthy blood donors (0/44) controls showed reactivities. Anti-mitochondrial autoantibodies (inner and outer membrane) were negative in ME/CFS cohort. Anti-cardiolipin antibody levels in patients did not differ significantly from healthy blood donors. In conclusion, the impaired mitochondrial/metabolic dysfunction, observed in ME/CFS, cannot be explained by presence of circulating autoantibodies against the tested mitochondrial epitopes.

Identifiants

pubmed: 32296708
doi: 10.3389/fmed.2020.00108
pmc: PMC7136523
doi:

Types de publication

Journal Article

Langues

eng

Pagination

108

Informations de copyright

Copyright © 2020 Nilsson, Palmer, Apostolou, Gottfries, Rizwan, Dahle and Rosén.

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Auteurs

Isabell Nilsson (I)

Division of Cell Biology, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.

Jeremy Palmer (J)

The Medical School, The University Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom.

Eirini Apostolou (E)

Division of Cell Biology, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.

Carl-Gerhard Gottfries (CG)

The Gottfries Clinic AB, Mölndal, Sweden.

Muhammad Rizwan (M)

Division of Cell Biology, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.

Charlotte Dahle (C)

Division of Cell Biology, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.

Anders Rosén (A)

Division of Cell Biology, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.

Classifications MeSH