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Article ; Online: Redox regulation of the immune response.

Morris, Gerwyn / Gevezova, Maria / Sarafian, Victoria / Maes, Michael

2022 Volume 19, Issue 10, Page(s) 1079–1101

Abstract: The immune-inflammatory response is associated with increased nitro-oxidative stress. The aim of this mechanistic review is to examine: (a) the role of redox-sensitive transcription factors and enzymes, ROS/RNS production, and the activity of cellular ... ...

Abstract	The immune-inflammatory response is associated with increased nitro-oxidative stress. The aim of this mechanistic review is to examine: (a) the role of redox-sensitive transcription factors and enzymes, ROS/RNS production, and the activity of cellular antioxidants in the activation and performance of macrophages, dendritic cells, neutrophils, T-cells, B-cells, and natural killer cells; (b) the involvement of high-density lipoprotein (HDL), apolipoprotein A1 (ApoA1), paraoxonase-1 (PON1), and oxidized phospholipids in regulating the immune response; and (c) the detrimental effects of hypernitrosylation and chronic nitro-oxidative stress on the immune response. The redox changes during immune-inflammatory responses are orchestrated by the actions of nuclear factor-κB, HIF1α, the mechanistic target of rapamycin, the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, mitogen-activated protein kinases, 5' AMP-activated protein kinase, and peroxisome proliferator-activated receptor. The performance and survival of individual immune cells is under redox control and depends on intracellular and extracellular levels of ROS/RNS. They are heavily influenced by cellular antioxidants including the glutathione and thioredoxin systems, nuclear factor erythroid 2-related factor 2, and the HDL/ApoA1/PON1 complex. Chronic nitro-oxidative stress and hypernitrosylation inhibit the activity of those antioxidant systems, the tricarboxylic acid cycle, mitochondrial functions, and the metabolism of immune cells. In conclusion, redox-associated mechanisms modulate metabolic reprogramming of immune cells, macrophage and T helper cell polarization, phagocytosis, production of pro- versus anti-inflammatory cytokines, immune training and tolerance, chemotaxis, pathogen sensing, antiviral and antibacterial effects, Toll-like receptor activity, and endotoxin tolerance.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Anti-Bacterial Agents ; Anti-Inflammatory Agents ; Antioxidants/metabolism ; Antiviral Agents ; Apolipoprotein A-I/metabolism ; Aryldialkylphosphatase/metabolism ; Cytokines/metabolism ; Glutathione/metabolism ; Immunity ; Lipoproteins, HDL/metabolism ; Mitogen-Activated Protein Kinases/metabolism ; NF-kappa B/metabolism ; Oxidation-Reduction ; Peroxisome Proliferator-Activated Receptors/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species/metabolism ; Sirolimus ; Thioredoxins/metabolism ; Toll-Like Receptors/metabolism
Chemical Substances	Anti-Bacterial Agents ; Anti-Inflammatory Agents ; Antioxidants ; Antiviral Agents ; Apolipoprotein A-I ; Cytokines ; Lipoproteins, HDL ; NF-kappa B ; Peroxisome Proliferator-Activated Receptors ; Reactive Oxygen Species ; Toll-Like Receptors ; Thioredoxins (52500-60-4) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Aryldialkylphosphatase (EC 3.1.8.1) ; Glutathione (GAN16C9B8O) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2022-09-02
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/s41423-022-00902-0
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Zs.A 6681: Show issues

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Article: Potential therapeutic interventions based on the role of the endoplasmic reticulum stress response in progressive neurodegenerative diseases.

Puri, Basant K / Morris, Gerwyn

Neural regeneration research

2018 Volume 13, Issue 11, Page(s) 1887–1889

Language	English
Publishing date	2018-09-27
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.238614
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Article ; Online: Mechanisms Explaining Muscle Fatigue and Muscle Pain in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): a Review of Recent Findings.

Gerwyn, Morris / Maes, Michael

Current rheumatology reports

2017 Volume 19, Issue 1, Page(s) 1

Abstract: Purpose of review: Here, we review potential causes of muscle dysfunction seen in many patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) such as the effects of oxidative and nitrosative stress (O&NS) and mitochondrial impairments ...

Abstract	Purpose of review: Here, we review potential causes of muscle dysfunction seen in many patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) such as the effects of oxidative and nitrosative stress (O&NS) and mitochondrial impairments together with reduced heat shock protein production and a range of metabolic abnormalities. Recent findings: Several studies published in the last few years have highlighted the existence of chronic O&NS, inflammation, impaired mitochondrial function and reduced heat shock protein production in many patients with ME/CFS. These studies have also highlighted the detrimental effects of chronically elevated O&NS on muscle functions such as reducing the time to muscle fatigue during exercise and impairing muscle contractility. Mechanisms have also been revealed by which chronic O&NS and or impaired heat shock production may impair muscle repair following exercise and indeed the adaptive responses in the striated muscle to acute and chronic increases in physical activity. The presence of chronic O&NS, low-grade inflammation and impaired heat shock protein production may well explain the objective findings of increased muscle fatigue, impaired contractility and multiple dimensions of exercise intolerance in many patients with ME/CFS.
MeSH term(s)	Exercise/physiology ; Fatigue Syndrome, Chronic/complications ; Fatigue Syndrome, Chronic/physiopathology ; Heat-Shock Proteins/biosynthesis ; Humans ; Muscle Fatigue/physiology ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiopathology ; Myalgia/etiology ; Myalgia/physiopathology ; Nitrosation/physiology ; Oxidative Stress/physiology
Chemical Substances	Heat-Shock Proteins
Language	English
Publishing date	2017-01
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2057357-1
ISSN	1534-6307 ; 1523-3774
ISSN (online)	1534-6307
ISSN	1523-3774
DOI	10.1007/s11926-017-0628-x
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Zs.A 5531: Show issues

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Article ; Online: Is a diagnostic blood test for chronic fatigue syndrome on the horizon?

Maes, Michael / Rodriguez, Laura Andres / Morris, Gerwyn

Expert review of molecular diagnostics

2019 Volume 19, Issue 12, Page(s) 1049–1051

MeSH term(s)	Autoantibodies/blood ; Biomarkers/blood ; Cytokines/blood ; Evaluation Studies as Topic ; Fatigue Syndrome, Chronic/blood ; Fatigue Syndrome, Chronic/diagnosis ; Fatigue Syndrome, Chronic/immunology ; Humans ; Machine Learning
Chemical Substances	Autoantibodies ; Biomarkers ; Cytokines
Language	English
Publishing date	2019-10-18
Publishing country	England
Document type	Editorial
ZDB-ID	2112530-2
ISSN	1744-8352 ; 1473-7159
ISSN (online)	1744-8352
ISSN	1473-7159
DOI	10.1080/14737159.2020.1681976
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Article ; Online: Increased ACE2, sRAGE, and Immune Activation, but Lowered Calcium and Magnesium in COVID-19.

Al-Hakeim, Hussein Kadhem / Al-Jassas, Hawraa Kadhem / Morris, Gerwyn / Maes, Michael

Recent advances in inflammation & allergy drug discovery

2022 Volume 16, Issue 1, Page(s) 32–43

Abstract: Background: The characterization of new biomarkers that could help externally validate the diagnosis of COVID-19 and optimize treatments is extremely important. Many studies have established changes in immune-inflammatory and antibody levels, but few ... ...

Abstract	Background: The characterization of new biomarkers that could help externally validate the diagnosis of COVID-19 and optimize treatments is extremely important. Many studies have established changes in immune-inflammatory and antibody levels, but few studies measured the soluble receptor for the advanced glycation end product (sRAGE), angiotensin-converting enzyme 2 (ACE2), calcium, and magnesium in COVID-19. Objective: To evaluate serum advanced glycation end-product receptor (sRAGE) and angiotensin converting enzyme (ACE)2 and peripheral oxygen saturation (SpO2) and chest CT scan abnormalities (CCTA) in COVID-19. Methods: sRAGE, ACE2, interleukin (IL)-6, IL-10, C-reactive protein (CRP), calcium, magnesium, and albumin were measured in 60 COVID-19 patients and 30 healthy controls. Results: COVID-19 is characterized by significantly increased IL-6, CRP, IL-10, sRAGE, ACE2, and lowered SpO2, albumin, magnesium, and calcium. COVID-19 with CCTAs showed lower SpO Conclusion: The results show that immune-inflammatory and RAGE pathways biomarkers may be used as an external validating criterion for the diagnosis of COVID-19. Those pathways coupled with lowered SpO2, calcium, and magnesium are drug targets that may help reduce the consequences of COVID-19.
Language	English
Publishing date	2022-03-22
Publishing country	Netherlands
Document type	Journal Article
ISSN	2772-2716
ISSN (online)	2772-2716
DOI	10.2174/2772270816666220318103929
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Article ; Online: Inflammation and Nitro-oxidative Stress as Drivers of Endocannabinoid System Aberrations in Mood Disorders and Schizophrenia.

Morris, Gerwyn / Sominsky, Luba / Walder, Kenneth R / Berk, Michael / Marx, Wolfgang / Carvalho, André F / Bortolasci, Chiara C / Maes, Michael / Puri, Basant K

Molecular neurobiology

2022 Volume 59, Issue 6, Page(s) 3485–3503

Abstract: The endocannabinoid system (ECS) is composed of the endocannabinoid ligands anandamide (AEA) and 2-arachidonoylgycerol (2-AG), their target cannabinoid receptors ( ... ...

Abstract	The endocannabinoid system (ECS) is composed of the endocannabinoid ligands anandamide (AEA) and 2-arachidonoylgycerol (2-AG), their target cannabinoid receptors (CB
MeSH term(s)	Amidohydrolases/metabolism ; Depressive Disorder, Major ; Endocannabinoids/metabolism ; Humans ; Inflammation ; MicroRNAs/metabolism ; Monoacylglycerol Lipases/metabolism ; Oxidative Stress ; Receptor, Cannabinoid, CB1/genetics ; Receptor, Cannabinoid, CB1/metabolism ; Schizophrenia
Chemical Substances	Endocannabinoids ; MIRN139 microRNA, human ; MicroRNAs ; Receptor, Cannabinoid, CB1 ; Monoacylglycerol Lipases (EC 3.1.1.23) ; Amidohydrolases (EC 3.5.-)
Language	English
Publishing date	2022-03-26
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-022-02800-y
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Zs.A 2411: Show issues

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Article ; Online: The lipid paradox in neuroprogressive disorders: Causes and consequences.

Morris, Gerwyn / Berk, Michael / Walder, Ken / O'Neil, Adrienne / Maes, Michael / Puri, Basant K

Neuroscience and biobehavioral reviews

2021 Volume 128, Page(s) 35–57

Abstract: Chronic systemic inflammation is associated with an increased risk of cardiovascular disease in an environment of low low-density lipoprotein (LDL) and low total cholesterol and with the pathophysiology of neuroprogressive disorders. The causes and ... ...

Abstract	Chronic systemic inflammation is associated with an increased risk of cardiovascular disease in an environment of low low-density lipoprotein (LDL) and low total cholesterol and with the pathophysiology of neuroprogressive disorders. The causes and consequences of this lipid paradox are explored. Circulating activated neutrophils can release inflammatory molecules such as myeloperoxidase and the pro-inflammatory cytokines interleukin-1 beta, interleukin-6 and tumour necrosis factor-alpha. Since activated neutrophils are associated with atherosclerosis and cardiovascular disease and with major depressive disorder, bipolar disorder and schizophrenia, it seems reasonable to hypothesise that the inflammatory molecules released by them may act as mediators of the link between systemic inflammation and the development of atherosclerosis in neuroprogressive disorders. This hypothesis is tested by considering the association at a molecular level of systemic inflammation with increased LDL oxidation; increased small dense LDL levels; increased lipoprotein (a) concentration; secretory phospholipase A
MeSH term(s)	Atherosclerosis ; Cytokines ; Humans ; Inflammation ; Lipids ; Lipoproteins, LDL ; Neurodegenerative Diseases ; Neutrophils ; Peroxidase ; Phospholipases A2
Chemical Substances	Cytokines ; Lipids ; Lipoproteins, LDL ; Peroxidase (EC 1.11.1.7) ; Phospholipases A2 (EC 3.1.1.4)
Language	English
Publishing date	2021-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2021.06.017
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Zs.A 1371: Show issues

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Article ; Online: The Putative Use of Lithium in Alzheimer's Disease.

Morris, Gerwyn / Berk, Michael

Current Alzheimer research

2016 Volume 13, Issue 8, Page(s) 853–861

Abstract: Alzheimer`s disease is a progressive neurodegenerative illness characterized by the invariant existence of β-amyloid plaques and neurofibrillary tangles. Presently approved pharmaceutical approaches offer only marginal efficacy and as yet there is no ... ...

Abstract	Alzheimer`s disease is a progressive neurodegenerative illness characterized by the invariant existence of β-amyloid plaques and neurofibrillary tangles. Presently approved pharmaceutical approaches offer only marginal efficacy and as yet there is no effective treatment which reverses or arrests the disease. Thus far, drugs targeting any single aspect of disease pathology have proved to be a failure or at best provided very slight clinical benefit. The consistent failure of drugs targeting aspects of the Aβ cascade has questioned the causal role of this pathway. There is a growing appreciation that the pathogenesis of the illness is multifactorial with Amyloid Beta, Phosphorylated Tau (ptau), inflammation, mitochondrial dysfunction, calcium dyshomeostasis, heavy metal imbalances, and GSK-3 interact in a highly complex manner to provoke a selfsustaining spiraling cascade of pathology, driving disease progression. In the light of such complex pathology, the failure of drugs aimed a targeting single molecules is not surprising as such approaches are usually ineffective against other complex diseases with a multifactorial pathogenesis. Combination therapies or multi target drugs might be more effective in controlling such illnesses. The putative neuroprotective effects of Lithium are achieved via the positive modulation of numerous homeostatic mechanisms regulating autophagy, oxidative stress, inflammation, and mitochondrial dysfunction likely achieved by inhibiting GSK-3 and inositol-145 triphosphate. Data regarding efficacy in human trials and animal models of AD are mixed, but recent data using "microdose" lithium in mild cognitive impairment is encouraging, hence lithium could be a putative multi target treatment in these patients. However, additional well designed long-term trials are needed to confirm its efficacy and safety, given that long term use is necessary to achieve reasonable therapeutic benefit.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/immunology ; Alzheimer Disease/metabolism ; Animals ; Brain/drug effects ; Brain/immunology ; Brain/metabolism ; Humans ; Lithium Compounds/pharmacology ; Lithium Compounds/therapeutic use ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use
Chemical Substances	Lithium Compounds ; Neuroprotective Agents
Language	English
Publishing date	2016-01-25
Publishing country	United Arab Emirates
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2205170-3
ISSN	1875-5828 ; 1567-2050
ISSN (online)	1875-5828
ISSN	1567-2050
DOI	10.2174/1567205013666160219113112
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Article ; Online: The role of microglia in neuroprogressive disorders: mechanisms and possible neurotherapeutic effects of induced ketosis.

Morris, Gerwyn / Puri, Basant K / Maes, Michael / Olive, Lisa / Berk, Michael / Carvalho, Andre F

Progress in neuro-psychopharmacology & biological psychiatry

2020 Volume 99, Page(s) 109858

Abstract: A comprehensive review of molecular mechanisms involved in the promotion and maintenance of distinct microglia phenotypes is provided. The acquisition and perpetuation of predominantly pro-inflammatory microglial phenotypes have been implicated in the ... ...

Abstract	A comprehensive review of molecular mechanisms involved in the promotion and maintenance of distinct microglia phenotypes is provided. The acquisition and perpetuation of predominantly pro-inflammatory microglial phenotypes have been implicated in the pathophysiology of several neuroprogressive diseases and is associated with reduced ATP production via oxidative phosphorylation, increased ATP generation by glycolysis, elevated oxidative and nitrosative stress and other metabolic, inflammatory and hormonal insults. Microglia can also adopt a predominantly anti-inflammatory phenotypes with neuroprotective properties. Strategies that promote and maintain a predominantly anti-inflammatory phenotype may hold promise as novel therapeutic opportunities for neuroprogressive illness. Induced ketosis may promote a transition towards predominantly anti-inflammatory microglial states/phenotypes by several mechanisms, including inhibition of glycolysis and increased NAD
MeSH term(s)	Animals ; Brain/metabolism ; Brain/pathology ; Diet, Ketogenic/methods ; Humans ; Ketone Bodies/metabolism ; Ketosis/chemically induced ; Ketosis/metabolism ; Microglia/metabolism ; Microglia/physiology ; Neurodegenerative Diseases/diet therapy ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Neuroprotection/physiology
Chemical Substances	Ketone Bodies
Language	English
Publishing date	2020-01-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	781181-0
ISSN	1878-4216 ; 0278-5846
ISSN (online)	1878-4216
ISSN	0278-5846
DOI	10.1016/j.pnpbp.2020.109858
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Zs.A 1342: Show issues

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Article ; Online: Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop?

Morris, Gerwyn / Maes, Michael / Berk, Michael / Puri, Basant K

Metabolic brain disease

2019 Volume 34, Issue 2, Page(s) 385–415

Abstract: A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular ... ...

Abstract	A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals. The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities. Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation. The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next. Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.
MeSH term(s)	Fatigue Syndrome, Chronic/diagnosis ; Fatigue Syndrome, Chronic/immunology ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Mitochondria/immunology ; Mitochondria/metabolism ; Neuroimaging/methods ; Oxidation-Reduction ; Oxidative Stress/physiology
Language	English
Publishing date	2019-02-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632824-6
ISSN	1573-7365 ; 0885-7490
ISSN (online)	1573-7365
ISSN	0885-7490
DOI	10.1007/s11011-019-0388-6
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