Mitochondria and immunity in chronic fatigue syndrome

Anderson, Geoffrey M.; Maes, Michaël

doi:10.1016/j.pnpbp.2020.109976

Cited by 40 publications

(43 citation statements)

References 231 publications

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“…One possible consequence of viral infection could be longer term mitochondrial dysfunction, which could lead to a variety of symptoms. Mitochondrial function, and their relationship to immunity, is again becoming a focus for research in the chronic fatigue syndrome, which is still not completely understood [ 282 ]. This has been further supported by evidence of mitochondrial dysfunction in PBMCs of people with chronic fatigue syndrome [ 283 ].…”

Section: Implications Of Sars-cov-2 Modulation Of Mitochondrial Functmentioning

confidence: 99%

SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

Nunn

Guy²,

Brysch

et al. 2020

Immun Ageing

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Infection with SARs-COV-2 displays increasing fatality with age and underlying co-morbidity, in particular, with markers of the metabolic syndrome and diabetes, which seems to be associated with a “cytokine storm” and an altered immune response. This suggests that a key contributory factor could be immunosenescence that is both age-related and lifestyle-induced. As the immune system itself is heavily reliant on mitochondrial function, then maintaining a healthy mitochondrial system may play a key role in resisting the virus, both directly, and indirectly by ensuring a good vaccine response. Furthermore, as viruses in general, and quite possibly this new virus, have also evolved to modulate immunometabolism and thus mitochondrial function to ensure their replication, this could further stress cellular bioenergetics. Unlike most sedentary modern humans, one of the natural hosts for the virus, the bat, has to “exercise” regularly to find food, which continually provides a powerful adaptive stimulus to maintain functional muscle and mitochondria. In effect the bat is exposed to regular hormetic stimuli, which could provide clues on how to resist this virus. In this paper we review the data that might support the idea that mitochondrial health, induced by a healthy lifestyle, could be a key factor in resisting the virus, and for those people who are perhaps not in optimal health, treatments that could support mitochondrial function might be pivotal to their long-term recovery.

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Section: Implications Of Sars-cov-2 Modulation Of Mitochondrial Functmentioning

confidence: 99%

SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

Nunn

Guy²,

Brysch

et al. 2020

Immun Ageing

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“…Dysfunctional mitochondria and high levels of free radicals have also been linked to Beckwith–Wiedemann [ 57 ], Angelman [ 97 , 98 ], and Prader–Willi [ 99 ] syndromes, as well as autism [ 100 , 101 ] and schizophrenia [ 102 , 103 ]. In fact, they have been observed in virtually all mental afflictions [ 42 , 104 ], from chronic psychological stress [ 105 ] and fatigue [ 106 ] to Alzheimer’s and Parkinson’s disease [ 107 ].…”

Section: (Too Much) Mother Versus Fathermentioning

confidence: 99%

Mental Health, Mitochondria, and the Battle of the Sexes

Bressan

Krämer

2021

Biomedicines

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This paper presents a broad perspective on how mental disease relates to the different evolutionary strategies of men and women and to growth, metabolism, and mitochondria—the enslaved bacteria in our cells that enable it all. Several mental disorders strike one sex more than the other; yet what truly matters, regardless of one’s sex, is how much one’s brain is “female” and how much it is “male”. This appears to be the result of an arms race between the parents over how many resources their child ought to extract from the mother, hence whether it should grow a lot or stay small and undemanding. An uneven battle alters the child’s risk of developing not only insulin resistance, diabetes, or cancer, but a mental disease as well. Maternal supremacy increases the odds of a psychosis-spectrum disorder; paternal supremacy, those of an autism-spectrum one. And a particularly lopsided struggle may invite one or the other of a series of syndromes that come in pairs, with diametrically opposite, excessively “male” or “female” characteristics. By providing the means for this tug of war, mitochondria take center stage in steadying or upsetting the precarious balance on which our mental health is built.

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“…The AhR can regulate mitochondrial function by a number of mechanisms, including via the regulation of the melatonergic pathway. There is a growing appreciation of the role of the melatonergic pathway, including within mitochondria and the cytoplasm, in the regulation of mitochondrial function, which may be particularly important in immune cells [ 25 ]. The AhR can regulate the melatonergic pathway via a number of mechanisms, including 1) the induction of CYP1A1 and CYP1B1, with CYP1A1 increasing the metabolism of estrogen, whilst CYP1B1 leads to the ‘backward’ conversion of melatonin to its precursor, NAS, and thereby increasing the NAS/melatonin ratio [ 26 ]; and 2) AhR suppression of YWHAZ (14-3-3ζ/δ) [ 8 ], given that 14-3-3ζ/δ is necessary to stabilize the initial enzyme in the melatonergic pathway AANAT.…”

Section: Sars-cov-2 Entry and Pathophysiologymentioning

confidence: 99%

“…This may be exemplified in macrophages where autocrine melatonin switches M-like pro-inflammatory macrophages to an M2-like phagocytic phenotype [ 25 ]. As to how SPMs and autocrine melatonin interact to downregulate activation associated glycolysis, whilst upregulating OXPHOS will be important to determine.…”

Section: Ahr and Wider Covid-19 Pathophysiologymentioning

confidence: 99%

Aryl Hydrocarbon Receptor Role in Co-Ordinating SARS-CoV-2 Entry and Symptomatology: Linking Cytotoxicity Changes in COVID-19 and Cancers; Modulation by Racial Discrimination Stress

Anderson¹,

Carbone

Mazzoccoli

2020

Biology

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There is an under-recognized role of the aryl hydrocarbon receptor (AhR) in co-ordinating the entry and pathophysiology of the severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) that underpins the COVID-19 pandemic. The rise in pro-inflammatory cytokines during the ‘cytokine storm’ induce indoleamine 2,3-dioxygenase (IDO), leading to an increase in kynurenine that activates the AhR, thereby heightening the initial pro-inflammatory cytokine phase and suppressing the endogenous anti-viral response. Such AhR-driven changes underpin the heightened severity and fatality associated with pre-existent high-risk medical conditions, such as type II diabetes, as well as to how racial discrimination stress contributes to the raised severity/fatality in people from the Black Asian and Minority Ethnic (BAME) communities. The AhR is pivotal in modulating mitochondrial metabolism and co-ordinating specialized, pro-resolving mediators (SPMs), the melatonergic pathways, acetyl-coenzyme A, and the cyclooxygenase (COX) 2-prostaglandin (PG) E2 pathway that underpin ‘exhaustion’ in the endogenous anti-viral cells, paralleling similar metabolic suppression in cytolytic immune cells that is evident across all cancers. The pro-inflammatory cytokine induced gut permeability/dysbiosis and suppression of pineal melatonin are aspects of the wider pathophysiological underpinnings regulated by the AhR. This has a number of prophylactic and treatment implications for SARS-CoV-2 infection and cancers and future research directions that better investigate the biological underpinnings of social processes and how these may drive health disparities.

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Mitochondria and immunity in chronic fatigue syndrome

Cited by 40 publications

References 231 publications

SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

Mental Health, Mitochondria, and the Battle of the Sexes

Aryl Hydrocarbon Receptor Role in Co-Ordinating SARS-CoV-2 Entry and Symptomatology: Linking Cytotoxicity Changes in COVID-19 and Cancers; Modulation by Racial Discrimination Stress

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