Serum Immune Proteins in Moderate and Severe Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients

Hardcastle, Sharni Lee; Brenu, Ekua; Johnston, Samantha; Nguyen, Thao; Huth, Teilah Kathryn; Ramos, Sandra Bahia; Staines, Donald; Marshall‐Gradisnik, Sonya

doi:10.7150/ijms.12399

Cited by 31 publications

(36 citation statements)

References 53 publications

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“…However, we used a prospective, national-wide, population-based cohort study to investigate the incidence of CFS and the risk of developing CFS among DES patients. We also considered whether CFS-related symptoms and comorbidities, such as immune dysregulation, overlapped [ 41 – 44 ]. The results showed that patients with any comorbidity had a higher risk of developing CFS.…”

Section: Discussionmentioning

confidence: 99%

Dry eye syndrome and the subsequent risk of chronic fatigue syndrome—a prospective population-based study in Taiwan

et al. 2018

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Background and AimThe clinical association between dry eye syndrome (DES) and chronic fatigue syndrome (CFS) remain unclear with less evidences. We aimed to investigate the relationship between CFS and DES using a national insurance and prospective cohort study.MethodsData from the Longitudinal Health Insurance Database 2000 was applied to estimate the incidence of CFS among patients with DES, and their age- and sex-matched controls without DES over a long-term follow-up period. All participants were CFS free at baseline, before the interval (2005–2007), but were later diagnosed with CFS. DES patients and its relative matched controls were excluded prevalent CFS before the same interval.ResultsWe identified 884 patients with DES and 3,536 matched controls in baseline and estimated the hazard ratios for incident CFS in the follow-up period. Patients with DES had a 2.08-fold considerably increasing risk of developing CFS, compared to non-DES group. An elevated risk of developing CFS remained (1.61-fold risk) even after adjusting for age, sex, and comorbidities. There was a presence of increasing risk in DES-related CFS when CFS-related comorbidities existing (adjusted hazard ratio, 1.98, 95% confidence interval, 1.19–3.29; p < 0.01). The subsequent risk for CFS between DES and non-DES patients was significant increased with three or more annual medical visits, the adjusted risk for CFS was 4.88-fold risk (95% CI, 2.26–10.58, p < 0.001).ConclusionWe recommended that physicians should be aware of the increased risk of CFS among DES patients and adequately assess the health impacts among these patients.

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Section: Discussionmentioning

confidence: 99%

Dry eye syndrome and the subsequent risk of chronic fatigue syndrome—a prospective population-based study in Taiwan

et al. 2018

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“…Many putative causes of CFS have been investigated but the absence of an agreed pathogenesis impacts the development of effective diagnostics and treatments. It is likely that multiple factors contribute which involve a number of interacting biological, environmental, and psychosocial factors [ 1 , 2 , 5 , 7 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

Reduction of Glucocorticoid Receptor Function in Chronic Fatigue Syndrome

Lynn

Maclachlan

Finkelmeyer

et al. 2018

Mediators of Inflammation

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Glucocorticoid receptor (GR) function may have aetiopathogenic significance in chronic fatigue syndrome (CFS), via its essential role in mediating inflammatory responses as well as in hypothalamic-pituitary-adrenal axis regulation. GR function can be estimated ex vivo by measuring dexamethasone (dex) modulation of cytokine response to lipopolysaccharide (LPS), and in vivo using the impact of dex on cortisol levels. This study aimed to compare the GR function between CFS (n = 48), primary Sjögren's syndrome (a disease group control) (n = 27), and sedentary healthy controls (HCs) (n = 20), and to investigate its relationship with clinical measures. In the GR ex vivo response assay, whole blood was diluted and incubated with LPS (to stimulate cytokine production), with or without 10 or 100 nanomolar concentrations of dex. Cytometric bead array (CBA) and flow cytometry enabled quantification of cytokine levels (TNFα, interleukin- (IL-) 6, and IL-10) in the supernatants. In the in vivo response assay, five plasma samples were taken for determination of total cortisol concentration using ELISA at half-hourly intervals on two consecutive mornings separated by ingestion of 0.5 mg of dex at 11 pm. The association of the data from the in vivo and ex vivo analyses with reported childhood adversity was also examined. CFS patients had reduced LPS-induced IL-6 and TNFα production compared to both control groups and reduced suppression of TNFα by the higher dose of dex compared to HCs. Cortisol levels, before or after dex, did not differ between CFS and HCs. Cortisol levels were more variable in CFS than HCs. In the combined group (CFS plus HC), cortisol concentrations positively and ex vivo GR function (determined by dex-mediated suppression of IL-10) negatively correlated with childhood adversity score. The results do not support the hypothesis that GR dysregulation is aetiopathogenic in CFS and suggest that current and future endocrine cross-sectional studies in CFS may be vulnerable to the confounding influence of childhood trauma which is likely increased by comorbid depression.

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“…In this context, a consistent systematic review was conducted by Blundell [137], and the third study could not find any differences between patients and controls for either IL-1β or IL-1α in a group of 100 patients and 79 controls [138].…”

Section: Evidence Of Microglial Activation and Pro-inflammatory Cytokmentioning

confidence: 93%

Shared Microglial Mechanisms Underpinning Depression and Fatigue and Their Comorbidities

Ajm¹,

Ds²,

Df³

et al. 2019

Preprint

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In 2011, it was reviewed that there is a strong co-occurrence between major depression and chronic fatigue syndrome (CFS), with fatigue and physio-somatic symptoms being key symptoms of depression, and depressive symptoms appearing during the course of CFS. Moreover, the comorbidity between both conditions may in part be explained by activated immune-inflammatory pathways, including increased translocation of Gram-negative bacteria and increased levels of pro-inflammatory cytokines, such as interleukin (IL)-1. Nevertheless, the possible involvement of activated microglia in this comorbidity has remained unclear. This paper aims to review microglial disturbances in major depression, CFS and their comorbidity. A comprehensive literature search was conducted using the PubMed / MEDLINE database to identify studies that are relevant to this current review. Depressed patients present neuroinflammatory alterations, probably related to microglial activation, while animal models show that a microglial response to immune challenges including lipopolysaccharides is accompanied by depressive-like behaviors. Recent evidence from preclinical studies indicate that activated microglia have a key role in the onset of fatigue. In chronic inflammatory conditions, such as infections and senescence, microglia orchestrate an inflammatory microenvironment thereby causing fatigue. In conclusion, based on our review we may posit that shared immune-inflammatory pathways and activated microglia underpin comorbid depression and CFS and that activated microglia are the main orchestrators of this comorbidity. As such, microglial activation and neuro-inflammation may be promising targets to treat the overlapping manifestations of both depression and CFS.

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Serum Immune Proteins in Moderate and Severe Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients

Cited by 31 publications

References 53 publications

Dry eye syndrome and the subsequent risk of chronic fatigue syndrome—a prospective population-based study in Taiwan

Dry eye syndrome and the subsequent risk of chronic fatigue syndrome—a prospective population-based study in Taiwan

Reduction of Glucocorticoid Receptor Function in Chronic Fatigue Syndrome

Shared Microglial Mechanisms Underpinning Depression and Fatigue and Their Comorbidities

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