scholarly journals Exosome-associated Mitochondrial DNA is Elevated in Patients with ME/CFS and Stimulates Human Cultured Microglia to Secrete IL-1β

2021 ◽  
Author(s):  
Theoharis C Theoharides ◽  
Irene Tsilioni ◽  
Benjamin Natelson
Keyword(s):  
Mitochondrial Dna ◽  
Sleep Disturbances ◽  
Serum Levels ◽  
Chronic Fatigue ◽  
Human Microglia ◽  
Fatigue Syndrome ◽  
Before And After ◽  
Pathogenetic Factor ◽  
Cognitive Problems ◽  
Potential Biomarkers

Abstract Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating disease that presents with fatigue, sleep disturbances, malaise and cognitive problems. The pathogenesis of ME/CFS is presently unknown and serum levels of potential biomarkers have been inconsistent. Methods: Exosomes were purified from serum obtained from patients with ME/CFS before and after exercise and their content of mitochondrial DNA (mtDNA) was determined by quantitative PCR. Exosomes from both patients and controls were incubated with cultured human microglia and release of interleukin-1beta (IL-1β) was measured by ELISA.Results: Here we show that serum mtDNA, associated with exosomes, is increased in ME/CFS after exercise. Moreover, exosomes isolated from patients with ME/CFS stimulate significant secretion of IL-1β from cultured human microglia. Conclusion: These results provide evidence for a potential novel pathogenetic factor and target for treatment of ME/CFS.

scholarly journals Exosome-associated mitochondrial DNA from patients with ME/CFS stimulates human cultured microglia to release IL-1β

2021 ◽  
Author(s):  
Irene Tsilioni ◽  
Benjamin Natelson ◽  
Theoharis C. Theoharides
Keyword(s):  
Mitochondrial Dna ◽  
Sleep Disturbances ◽  
Serum Levels ◽  
Chronic Fatigue ◽  
Human Microglia ◽  
Fatigue Syndrome ◽  
Pathogenetic Factor ◽  
Significant Release ◽  
Cognitive Problems ◽  
Potential Biomarkers

Abstract Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating disease that presents with fatigue, sleep disturbances, malaise and cognitive problems. The pathogenesis of ME/CFS is presently unknown and serum levels of potential biomarkers have been inconsistent. Here we show that serum mitochondrial DNA (mtDNA), associated with exosomes, is increased in ME/CFS only after exercise. Moreover, exosomes isolated from patients with ME/CFS stimulate significant release of IL-1β from cultured human microglia. These results provide evidence for a potential novel pathogenetic factor and target for treatment of ME/CFS.

scholarly journals COVID-19 and post-infectious myalgic encephalomyelitis/chronic fatigue syndrome: a narrative review

2021 ◽  
Vol 8 ◽  
pp. 204993612110093
Author(s):  
Sonia Poenaru ◽  
Sara J. Abdallah ◽  
Vicente Corrales-Medina ◽  
Juthaporn Cowan
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Sleep Disturbances ◽  
Q Fever ◽  
Orthostatic Intolerance ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Exercise Intolerance ◽  
Laboratory Findings ◽  
Fatigue Syndrome ◽  
Post Infectious

Coronavirus disease 2019 (COVID-19) is a viral infection which can cause a variety of respiratory, gastrointestinal, and vascular symptoms. The acute illness phase generally lasts no more than 2–3 weeks. However, there is increasing evidence that a proportion of COVID-19 patients experience a prolonged convalescence and continue to have symptoms lasting several months after the initial infection. A variety of chronic symptoms have been reported including fatigue, dyspnea, myalgia, exercise intolerance, sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. These symptoms are similar to those seen in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a chronic multi-system illness characterized by profound fatigue, sleep disturbances, neurocognitive changes, orthostatic intolerance, and post-exertional malaise. ME/CFS symptoms are exacerbated by exercise or stress and occur in the absence of any significant clinical or laboratory findings. The pathology of ME/CFS is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. Although not exclusively considered a post-infectious entity, ME/CFS has been associated with several infectious agents including Epstein–Barr Virus, Q fever, influenza, and other coronaviruses. There are important similarities between post-acute COVID-19 symptoms and ME/CFS. However, there is currently insufficient evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies.

Unusual pattern of mitochondrial DNA deletions in skeletal muscle of an adult human with chronic fatigue syndrome

1995 ◽  
Vol 4 (4) ◽  
pp. 751-754 ◽  
Author(s):  
Chunfang Zhang ◽  
Alessandra Baumer ◽  
Ian R. Mackay ◽  
Anthony W. Linnane ◽  
Phillip Nagley
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dna ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Unusual Pattern ◽  
Adult Human ◽  
Fatigue Syndrome ◽  
Dna Deletions

scholarly journals Circulating extracellular vesicles as potential biomarkers in chronic fatigue syndrome/myalgic encephalomyelitis: an exploratory pilot study

2018 ◽  
Vol 7 (1) ◽  
pp. 1453730 ◽  
Author(s):  
Jesús Castro-Marrero ◽  
Esther Serrano-Pertierra ◽  
Myriam Oliveira-Rodríguez ◽  
Maria Cleofé Zaragozá ◽  
Alba Martínez-Martínez ◽  
...  
Keyword(s):  
Pilot Study ◽  
Chronic Fatigue Syndrome ◽  
Extracellular Vesicles ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Fatigue Syndrome ◽  
Potential Biomarkers

scholarly journals Interventions to treat pain in paediatric CFS/ME: a systematic review

2020 ◽  
Vol 4 (1) ◽  
pp. e000617
Author(s):  
Caitlin Ascough ◽  
Hayley King ◽  
Teona Serafimova ◽  
Lucy Beasant ◽  
Sophie Jackson ◽  
...  
Keyword(s):  
Specific Treatment ◽  
Chronic Fatigue ◽  
Cochrane Library ◽  
Fatigue Syndrome ◽  
Pain Scores ◽  
Before And After ◽  
Registration Number ◽  
Randomised Controlled ◽  
Detailed Search ◽  
The Cochrane Library

BackgroundPaediatric chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is common (prevalence 1%–2%). Two-thirds of children experience moderate or severe pain, which is associated with increased fatigue and poorer physical function. However, we do not know if treatment for CFS/ME improves pain.ObjectiveIdentify whether specialist treatment of paediatric CFS/ME improves pain.MethodsWe conducted a detailed search in MEDLINE, EMBASE, PsycINFO and the Cochrane Library. Two researchers independently screened texts published between 1994 and 24 January 2019 with no language restrictions. Inclusion criteria were (1) randomised controlled trials and observational studies; (2) participants aged <19 years with CFS/ME; and (3) measure of pain before and after an intervention.ResultsOf 1898 papers screened, 26 studies investigated treatment for paediatric CFS/ME, 19 of which did not measure pain at any time point. Only five treatment studies measured pain at baseline and follow-up and were included in this review. None of the interventions were specifically targeted at treating pain. Of the included studies, two showed no improvement in pain scores, one suggested an improvement in one subgroup and two studies identified improvements in pain measures in ‘recovered’ patients compared with ‘non-recovered’ patients.ConclusionsDespite the prevalence and impact of pain in children with CFS/ME surprisingly few treatment studies measured pain. In those that did measure pain, the treatments used focused on overall management of CFS/ME and we identified no treatments that were targeted specifically at managing pain. There is limited evidence that treatment helps improve pain scores. However, patients who recover appear to have less pain than those who do not recover. More studies are needed to determine if pain in paediatric CFS/ME requires a specific treatment approach, with a particular focus on patients who do not recover following initial treatment.PROSPERO registration numberCRD42019117540.

scholarly journals Detection of Urine Metabolites in a Rat Model of Chronic Fatigue Syndrome before and after Exercise

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Changzhuan Shao ◽  
Yiming Ren ◽  
Zinan Wang ◽  
Chenzhe Kang ◽  
Hongke Jiang ◽  
...  
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Rat Model ◽  
Steroid Hormone ◽  
Chronic Fatigue ◽  
Sphingolipid Metabolism ◽  
Urine Metabolites ◽  
Steroid Hormone Biosynthesis ◽  
Fatigue Syndrome ◽  
Before And After ◽  
Hormone Biosynthesis

Purpose. The aim of the present study was to elucidate the metabolic mechanisms associated with chronic fatigue syndrome (CFS) via an analysis of urine metabolites prior to and following exercise in a rat model. Methods. A rat model of CFS was established using restraint-stress, forced exercise, and crowded and noisy environments over a period of 4 weeks. Behavioral experiments were conducted in order to evaluate the model. Urine metabolites were analyzed via gas chromatography-mass spectrometry (GC-MS) in combination with multivariate statistical analysis before and after exercise. Results. A total of 20 metabolites were detected in CFS rats before and after exercise. Three metabolic pathways (TCA cycle; alanine, aspartate, and glutamate metabolism; steroid hormone biosynthesis) were significantly impacted before and after exercise, while sphingolipid metabolism alone exhibited significant alterations after exercise only. Conclusion. In addition to metabolic disturbances involving some energy substances, alterations in steroid hormone biosynthesis and sphingolipid metabolism were detected in CFS rats. Sphingosine and 21-hydroxypregnenolone may be key biomarkers of CFS, potentially offering evidence in support of immune dysfunction and hypothalamic-pituitary-adrenal (HPA) axis hypoactivity in patients with CFS.

scholarly journals Post-COVID Chronic Fatigue Syndrome: New Challenge Ahead

2021 ◽  
Vol 6 (3) ◽  
pp. 472-478
Author(s):  
Adwitiya Ray ◽  
Neharika Saini ◽  
Ravi Parkash
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Sleep Disturbances ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Exercise Intolerance ◽  
Multiple Systems ◽  
Fatigue Syndrome ◽  
History Of ◽  
Illness Phase ◽  
Post Infectious

Coronavirus disease 2019 (COVID-19) is a viral infection that causes various respiratory, gastrointestinal, and vascular symptoms. The acute illness phase lasts for about 2-3 weeks. However, there is increasing evidence that a percentage of COVID-19 patients continue to experience long-lasting symptoms characterized by fatigue, dyspnea, myalgia, exercise intolerance, and sleep disturbances, difficulty concentrating, anxiety, fever, headache, malaise, and vertigo. Similar symptoms are reported by patients who having myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS). ME/CFS pathology is not known: it is thought to be multifactorial, resulting from the dysregulation of multiple systems in response to a particular trigger. There is a resemblance between post-acute COVID-19 symptoms and ME/CFS. However, at present, there is inadequate evidence to establish COVID-19 as an infectious trigger for ME/CFS. Further research is required to determine the natural history of this condition, as well as to define risk factors, prevalence, and possible interventional strategies. Keywords: chronic fatigue syndrome, COVID-19, human coronavirus, myalgic encephalomyelitis, post-infectious fatigue, review.

scholarly journals Differential heat shock protein responses to strenuous standardized exercise in chronic fatigue syndrome patients and matched healthy controls

2008 ◽  
Vol 31 (6) ◽  
pp. 319 ◽  
Author(s):  
Anita A Thambirajah ◽  
Kenna Sleigh ◽  
H. Grant Stiver ◽  
Anthony W Chow
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Chronic Fatigue Syndrome ◽  
Mononuclear Cells ◽  
Chronic Fatigue ◽  
Peripheral Blood Mononuclear ◽  
Post Exercise ◽  
Fatigue Syndrome ◽  
Before And After ◽  
Biologic Marker

Purpose: Since physical exertion is known to exacerbate the symptoms of chronic fatigue syndrome (CFS) and metabolic changes and including oxidative stress can modulate heat shock protein (HSP) expression responses, we sought to determine whether HSP expression is altered in CFS patients before and after exercise. Heat shock proteins (HSPs) in peripheral blood mononuclear cells (PBMC) were examined from 6 chronic fatigue syndrome (CFS) patients and 7 controls before and after a standardized treadmill exercise. Basal hsp27 was significantly higher among CFS patients compared to controls, and decreased immediately post-exercise, remaining below basal levels even at 7 days. A similar pattern was observed for HSP60, which gradually decreased in CFS patients but increased in controls post-exercise. These findings suggest an abnormal adaptive response to oxidative stress in CFS, and raise the possibility that HSP profiling may provide a more objective biologic marker for this illness. Methods: HSP27, HSP60, HSP70 and HSP90 expression from 6 CFS patients and 7 age- and sex-matched controls were examined by western blot analysis of peripheral blood mononuclear cells immediately before, after, and at 1 day and 7 days following a standardized treadmill exercise. Results: Basal HSP27 was higher among CFS patients than in controls (0.54 ± 0.13 vs. 0.19 ± 0.06, mean ± SEM; P < 0.01). In addition, these levels in CFS patients decreased immediately post-exercise (0.25 ± 0.09; P < 0.05) and remained below basal levels at day 1 post-exercises (0.18 ± 0.05; P < 0.05). P < 0.05). This declining expression of HSP27 during the post-exercise period among CFS patients was confirmed by one-way ANOVA analysis with repeated measures (P < 0.05). In contrast, HSP27 levels remained relatively constant following exercise among control subjects. Similar patterns of declining HSP levels in CFS patients were also observed for HSP60 (0.94 ± 0.40 vs. 1.32 ± 0.46; P < 0.05), and for HSP90 (0.34 ± 0.09 vs. 0.49 ± 0.10; P < 0.05) at day 7 post-exercise compared with basal levels, respectively. In contrast, HSP60 levels in control subjects increased at day 1 (1.09 ± 0.27) and day 7 (1.24 ± 0.50) post-exercise compared to corresponding levels immediately post-exercise (0.55 ± 0.06) (P < 0.05, respectively). Conclusion: These preliminary findings suggest an abnormal or defective adaptive response to oxidative stress in CFS, and raise the possibility that HSP profiling may provide a more objective biologic marker for this illness.

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