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
Abstract
:1. Introduction
The Aryl Hydrocarbon Receptor
2. SARS-CoV-2 Entry and Pathophysiology
2.1. Entry
2.2. Pathophysiology
2.3. Cytokine Storm Consequences
2.4. AhR Regulation of Mitochondrial Metabolism
2.5. AhR and Pre-Existing High-Risk COVID-19 Medical Conditions
2.6. AhR and Stress
2.7. Stress and the Gut
3. AhR and Wider COVID-19 Pathophysiology
3.1. AhR, Platelets, ROCK, and SARS-CoV-2 Severity/Fatality
3.2. AhR, Acetyl-CoA, COX2, and Specialized Pro-Resolving Mediators (SPMs)
3.3. AhR, COX2, SPMs, Acetyl-CoA, and miR-155
3.4. Gut Dysbiosis: Interactions with Acetyl-CoA, COX2, SPMs, and AhR
4. Integrating Racial Discrimination into SARS-CoV-2 Pathophysiology
5. Treatment Implications
5.1. AhR Antagonists
5.1.1. Vitamin B12 and Folic Acid
5.1.2. Green Tea Polyphenols
5.2. Melatonin
5.3. ROCK Inhibitors
5.4. IDO Inhibitors
5.5. Nimesulide
5.6. Prophylaxis
5.7. Treatment
6. Future Research
7. Conclusions
Author Contributions
Funding
Conflicts of Interest
Abbreviations
α7nAChR | alpha 7 nicotinic acetylcholine receptor |
Aβ | amyloid-beta |
AANAT | aralkylamine N-acetyltransferase |
ACC | acetyl-CoA carboxylase |
ACE2r | angiotensin-converting enzyme 2 receptor |
acetyl-CoA | acetyl-coenzyme A |
AhR | aryl hydrocarbon receptor |
BAME | Black Asian and Minority Ethnic |
CD8+ | cluster of differentiation 8 |
COVID-19 | coronavirus disease-19 |
COX2 | cyclooxygenase 2 |
CRH | corticotropin-releasing hormone |
CVD | cardiovascular disease |
CYP | cytochdrome P450 |
DPP-4 | Dipeptidyl peptidase 4 |
EGCG | epigallocatechin gallate |
EP4 | prostaglandin E2 receptor 4 |
HMGB | high-mobility group box |
IDO | indoleamine 2,3-dioxygenase |
IFN | interferons |
IL | interleukin |
LPS | lipopolysaccharide |
MDSC | myeloid-derived suppressor cells |
N-ASph | N-acetylsphingosine |
NAS | N-acetylserotonin |
NK | natural killer |
OXPHOS | oxidative phosphorylation |
PDC | pyruvate dyhydroganse complex |
PDK | pyruvate dehydrogenase kinase |
PGE2 | prostaglandin E2 |
ROCK | RhoA-associated kinase |
S1P | sphingosine-1-phosphate |
SARS-CoV-2 | Severe Acute Respiratory Syndrome associatedcoronavirus |
SNP | single nucleotide polymorphism |
SOD | superoxide dismutase |
SphK | sphingosine kinase |
SPM | specialized pro-resolving mediators |
TCA | tricarboxylic acid |
TCDD | 2,3,7,8-tetrachlorodibenzo-p-dioxin |
TDO | tryptophan 2,3-dioxygenase |
TLR | toll-like receptor |
TNF | tumor necrosis factor |
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Treatment | Mode of Efficacy | References |
---|---|---|
Vitamin B12/Folate | AhR antagonism; could inhibit entry, cytokine storm and enhance antiviral response | [123] |
Vitamin B12 | Mpro protease inhibitor; expect to inhibit entry | [124] |
Optimizes NK cell cytotoxicity | [125] | |
Resveratrol, Curcumin and Rosiglitazone | Inhibitors of the IDO-kynurenine-AhR pathway | [122] |
Green Tea’s-Epigallocatechin gallate (EGCG) | AhR antagonist | [127] |
- EGCG | MDSC inhibitor; increases CD8+ T cell cytotoxicity | [128] |
- EGCG, epicatechingallate and gallocatechin-3-gallate | Mpro antagonist | [133,134] |
- EGCG | Inhibits monoamine oxidase; increases 14-3-3 and therefore melatonergic pathway | [135,136] |
- EGCG | Induces M2-like macrophage;dampens neutrophils | [140] |
- tannic acid | PKM2 inhibitor; enhance NK cell cytotoxicity? | [141] |
- caffeine | Adenosine A2A receptor inhibition increases CD8+ T cell and NK cell cytotoxicity | [155] |
Melatonin | Inhibits SARS-CoV-2 infection risk | [147,148] |
Increases α7nAChR levels, dampening immune activation | [27] | |
Decreases platelet activation | [20] | |
Seems to reset immune cell metabolism | [5] | |
ROCK inhibitors: Y27632 | Only Y27632 clinically available but toxicity problematic; efficacy via S1P3r/RhoA/ROCK inhibition | [151] |
Curcumin | Acts indirectly to inhibit ROCK pathway | [153] |
IDO inhibitors | Potential, but not currently indicated | [154] |
Nimesulide | Inhibitor of B0AT1/SLC6A19 and therefore potentially of entry via the ACE2-B0AT1 dimer | [10] |
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Anderson, G.; Carbone, A.; Mazzoccoli, G. 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. Biology 2020, 9, 249. https://doi.org/10.3390/biology9090249
Anderson G, Carbone A, Mazzoccoli G. 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. Biology. 2020; 9(9):249. https://doi.org/10.3390/biology9090249
Chicago/Turabian StyleAnderson, George, Annalucia Carbone, and Gianluigi Mazzoccoli. 2020. "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" Biology 9, no. 9: 249. https://doi.org/10.3390/biology9090249