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1.
Oxid Med Cell Longev ; 2022: 5397733, 2022.
Article in English | MEDLINE | ID: covidwho-1635531

ABSTRACT

The infection of coronavirus disease (COVID-19) seriously threatens human life. It is urgent to generate effective and safe specific antibodies (Abs) against the pathogenic elements of COVID-19. Mice were immunized with SARS-CoV-2 spike protein antigens: S ectodomain-1 (CoV, in short) mixed in Alum adjuvant for 2 times and boosted with CoV weekly for 6 times. A portion of mice were treated with Maotai liquor (MTL, in short) or/and heat stress (HS) together with CoV boosting. We observed that the anti-CoV Ab was successfully induced in mice that received the CoV/Alum immunization for 2 times. However, upon boosting with CoV, the CoV Ab production diminished progressively; spleen CoV Ab-producing plasma cell counts reduced, in which substantial CoV-specific Ab-producing plasma cells (sPC) were apoptotic. Apparent oxidative stress signs were observed in sPCs; the results were reproduced by exposing sPCs to CoV in the culture. The presence of MTL or/and HS prevented the CoV-induced oxidative stress in sPCs and promoted and stabilized the CoV Ab production in mice in re-exposure to CoV. In summary, CoV/Alum immunization can successfully induce CoV Ab production in mice that declines upon reexposure to CoV. Concurrent administration of MTL/HS stabilizes and promotes the CoV Ab production in mice.


Subject(s)
Antibodies, Neutralizing/biosynthesis , Antibodies, Viral/biosynthesis , Apoptosis , COVID-19/immunology , Plasma Cells/immunology , SARS-CoV-2/physiology , Superoxide Dismutase-1/physiology , Adjuvants, Immunologic , Alcoholic Beverages , Alum Compounds , Angiotensin-Converting Enzyme 2/physiology , Animals , Antibodies, Neutralizing/blood , Antibodies, Viral/blood , COVID-19/enzymology , COVID-19 Vaccines/immunology , Heat-Shock Response , Immunization, Secondary , Immunogenicity, Vaccine , Janus Kinase 2/physiology , Male , Mice , Mice, Inbred C57BL , Oxidative Stress , Plasma Cells/drug effects , Plasma Cells/pathology , Reactive Oxygen Species/metabolism , STAT1 Transcription Factor/physiology , Signal Transduction , Specific Pathogen-Free Organisms , Spike Glycoprotein, Coronavirus/immunology , Vaccination
2.
Bull Exp Biol Med ; 172(3): 283-287, 2022 Jan.
Article in English | MEDLINE | ID: covidwho-1611428

ABSTRACT

We studied laboratory parameters of patients with COVID-19 against the background of chronic pathologies (cardiovascular pathologies, obesity, type 2 diabetes melitus, and cardiovascular pathologies with allergy to statins). A decrease in pH and a shift in the electrolyte balance of blood plasma were revealed in all studied groups and were most pronounced in patients with cardiovascular pathologies with allergy to statin. It was found that low pH promotes destruction of lipid components of the erythrocyte membranes in patients with chronic pathologies, which was seen from a decrease in Na+/K+-ATPase activity and significant hyponatrenemia. In patients with cardiovascular pathologies and allergy to statins, erythrocyte membranes were most sensitive to a decrease in pH, while erythrocyte membranes of obese patients showed the greatest resistance to low pH and oxidative stress.


Subject(s)
COVID-19/complications , Hyponatremia/etiology , Hypoxia/complications , Sodium-Potassium-Exchanging ATPase/physiology , Aged , COVID-19/metabolism , Cardiovascular Diseases/complications , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/virology , Case-Control Studies , Chronic Disease , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/virology , Drug Hypersensitivity/complications , Drug Hypersensitivity/metabolism , Drug Hypersensitivity/virology , Erythrocyte Membrane/metabolism , Erythrocytes/metabolism , Female , Fluid Shifts/physiology , Humans , Hydrogen-Ion Concentration , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , Hyponatremia/metabolism , Hyponatremia/virology , Hypoxia/metabolism , Lipid Peroxidation/physiology , Male , Middle Aged , Obesity/complications , Obesity/metabolism , Obesity/virology , Oxidative Stress/physiology , SARS-CoV-2/physiology , Sodium/metabolism , Stress, Physiological/physiology
3.
Bratisl Lek Listy ; 123(1): 9-15, 2022.
Article in English | MEDLINE | ID: covidwho-1598443

ABSTRACT

BACKGROUND: After an acute treatment for coronavirus disease (COVID-19), some symptoms may persist for several weeks, for example: fatigue, headaches, muscle and joint pain, cough, loss of taste and smell, sleep and memory disturbances, depression. Many viruses manipulate mitochondrial function, but the exact mechanisms of SARS-CoV-2 virus effect remain unclear. We tested the hypothesis that SARS-CoV-2 virus may affect mitochondrial energy production and endogenous biosynthesis of coenzyme Q10 (CoQ10). METHODS: Ten patients after COVID-19 and 15 healthy individuals were included in the study. Platelets isolated from peripheral blood were used as an accessible source of mitochondria. High-resolution respirometry for the evaluation of platelets mitochondrial function, and HPLC method for CoQ10 determination were used. Oxidative stress was evaluated by TBARS concentration in plasma. RESULTS: Platelet mitochondrial respiratory chain function, oxidative phosphorylation and endogenous CoQ10 level were reduced in the patients after COVID-19. CONCLUSION: We assume that a reduced concentration of endogenous CoQ10 may partially block electron transfer in the respiratory chain resulting in a reduced adenosine triphosphate (ATP) production in the patients after COVID-19. Targeted mitochondrial therapy with CoQ10 supplementation and spa rehabilitation may improve mitochondrial health and accelerate the recovery of the patients after COVID-19. Platelet mitochondrial function and CoQ10 content may be useful mitochondrial health biomarkers after SARS-CoV-2 infection (Tab. 3, Fig. 3, Ref. 46).


Subject(s)
COVID-19 , Humans , Mitochondria/metabolism , Oxidative Stress , SARS-CoV-2 , Ubiquinone/analogs & derivatives , Ubiquinone/metabolism
4.
Biochim Biophys Acta Mol Basis Dis ; 1868(3): 166321, 2022 03 01.
Article in English | MEDLINE | ID: covidwho-1588240

ABSTRACT

SARS-CoV-2 causes coronavirus disease 2019 (COVID-19) also in pregnant women. Infection in pregnancy leads to maternal and placental functional alterations. Pregnant women with vascular defects such as preeclampsia show high susceptibility to SARS-CoV-2 infection by undefined mechanisms. Pregnant women infected with SARS-CoV-2 show higher rates of preterm birth and caesarean delivery, and their placentas show signs of vasculopathy and inflammation. It is still unclear whether the foetus is affected by the maternal infection with this virus and whether maternal infection associates with postnatal affections. The SARS-CoV-2 infection causes oxidative stress and activation of the immune system leading to cytokine storm and next tissue damage as seen in the lung. The angiotensin-converting-enzyme 2 expression is determinant for these alterations in the lung. Since this enzyme is expressed in the human placenta, SARS-CoV-2 could infect the placenta tissue, although reported to be of low frequency compared with maternal lung tissue. Early-onset preeclampsia (eoPE) shows higher expression of ADAM17 (a disintegrin and metalloproteinase 17) causing an imbalanced renin-angiotensin system and endothelial dysfunction. A similar mechanism seems to potentially account for SARS-CoV-2 infection. This review highlights the potentially common characteristics of pregnant women with eoPE with those with COVID-19. A better understanding of the mechanisms of SARS-CoV-2 infection and its impact on the placenta function is determinant since eoPE/COVID-19 association may result in maternal metabolic alterations that might lead to a potential worsening of the foetal programming of diseases in the neonate, young, and adult.


Subject(s)
COVID-19/physiopathology , COVID-19/virology , Oxidative Stress/physiology , Pre-Eclampsia/physiopathology , Pre-Eclampsia/virology , Animals , Female , Humans , Pregnancy , SARS-CoV-2/pathogenicity
5.
Int Immunopharmacol ; 103: 108463, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1587490

ABSTRACT

Therapeutics that impair the innate immune responses of the liver during the inflammatory cytokine storm like that occurring in COVID-19 are greatly needed. Much interest is currently directed toward Janus kinase (JAK) inhibitors as potential candidates to mitigate this life-threatening complication. Accordingly, this study investigated the influence of the novel JAK inhibitor ruxolitinib (RXB) on concanavalin A (Con A)-induced hepatitis and systemic hyperinflammation in mice to simulate the context occurring in COVID-19 patients. Mice were orally treated with RXB (75 and 150 mg/kg) 2 h prior to the intravenous administration of Con A (20 mg/kg) for a period of 12 h. The results showed that RXB pretreatments were efficient in abrogating Con A-instigated hepatocellular injury (ALT, AST, LDH), necrosis (histopathology), apoptosis (cleaved caspase-3) and nuclear proliferation due to damage (PCNA). The protective mechanism of RXB were attributed to i) prevention of Con A-enhanced hepatic production and systemic release of the proinflammatory cytokines TNF-α, IFN-γ and IL-17A, which coincided with decreasing infiltration of immune cells (monocytes, neutrophils), ii) reducing Con A-induced hepatic overexpression of IL-1ß and CD98 alongside NF-κB activation, and iii) lessening Con A-induced consumption of GSH and GSH peroxidase and generation of oxidative stress products (MDA, 4-HNE, NOx) in the liver. In summary, JAK inhibition by RXB led to eminent protection of the liver against Con A-deleterious manifestations primarily via curbing the inflammatory cytokine storm driven by TNF-α, IFN-γ and IL-17A.


Subject(s)
Concanavalin A/toxicity , Cytokine Release Syndrome/chemically induced , Cytokine Release Syndrome/drug therapy , Nitriles/pharmacology , Pyrazoles/pharmacology , Pyrimidines/pharmacology , Aldehydes/metabolism , Animals , Chemical and Drug Induced Liver Injury , Dose-Response Relationship, Drug , Inflammation/chemically induced , Liver/drug effects , Liver/metabolism , Male , Malondialdehyde/metabolism , Mice , Mice, Inbred BALB C , Nitrates/metabolism , Nitriles/administration & dosage , Nitrites/metabolism , Oxidative Stress , Peroxidase/metabolism , Pyrazoles/administration & dosage , Pyrimidines/administration & dosage
6.
Int J Mol Sci ; 22(24)2021 Dec 19.
Article in English | MEDLINE | ID: covidwho-1580688

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) triggered the pandemic Coronavirus Disease 19 (COVID-19), causing millions of deaths. The elderly and those already living with comorbidity are likely to die after SARS-CoV-2 infection. People suffering from Alzheimer's disease (AD) have a higher risk of becoming infected, because they cannot easily follow health roles. Additionally, those suffering from dementia have a 40% higher risk of dying from COVID-19. Herein, we collected from Gene Expression Omnibus repository the brain samples of AD patients who died of COVID-19 (AD+COVID-19), AD without COVID-19 (AD), COVID-19 without AD (COVID-19) and control individuals. We inspected the transcriptomic and interactomic profiles by comparing the COVID-19 cohort against the control cohort and the AD cohort against the AD+COVID-19 cohort. SARS-CoV-2 in patients without AD mainly activated processes related to immune response and cell cycle. Conversely, 21 key nodes in the interactome are deregulated in AD. Interestingly, some of them are linked to beta-amyloid production and clearance. Thus, we inspected their role, along with their interactors, using the gene ontologies of the biological process that reveals their contribution in brain organization, immune response, oxidative stress and viral replication. We conclude that SARS-CoV-2 worsens the AD condition by increasing neurotoxicity, due to higher levels of beta-amyloid, inflammation and oxidative stress.


Subject(s)
Alzheimer Disease/genetics , COVID-19/complications , COVID-19/genetics , Alzheimer Disease/complications , Alzheimer Disease/virology , Amyloid beta-Peptides/metabolism , Brain/virology , COVID-19/physiopathology , Comorbidity/trends , Databases, Factual , Gene Expression/genetics , Gene Expression Profiling/methods , Humans , Inflammation/metabolism , Neurotoxicity Syndromes/metabolism , Oxidative Stress/physiology , Pandemics , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Transcriptome/genetics
7.
Inflammopharmacology ; 29(5): 1347-1355, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1557643

ABSTRACT

The natural pathway of antioxidant production is mediated through Kelch-like erythroid cell-derived protein with Cap and collar homology [ECH]-associated protein 1 (Keap1)-Nuclear factor erythroid 2-related factor 2 (Nrf2) system. Keap1 maintains a low level of Nrf2 by holding it in its protein complex. Also, Keap1 facilitates the degradation of Nrf2 by ubiquitination. In other words, Keap1 is a down-regulator of Nrf2. To boost the production of biological antioxidants, Keap1 has to be inhibited and Nrf2 has to be released. Liberated Nrf2 is in an unbound state, so it travels to the nucleus to stimulate the antioxidant response element (ARE) present on the antioxidant genes. AREs activate biosynthesis of biological antioxidants through genes responsible for the production of antioxidants. In some cases of coronavirus disease 2019 (COVID-19), there is an enormous release of cytokines. The antioxidant defense mechanism in the body helps in counteracting symptoms induced by the cytokine storm in COVID-19. So, boosting the production of antioxidants is highly desirable in such a condition. In this review article, we have compiled the role of Keap1-Nrf2 system in antioxidant production. We further propose its potential therapeutic use in managing cytokine storm in COVID-19.


Subject(s)
COVID-19/metabolism , COVID-19/therapy , Cytokine Release Syndrome/metabolism , Cytokine Release Syndrome/therapy , Kelch-Like ECH-Associated Protein 1/metabolism , NF-E2-Related Factor 2/metabolism , Animals , Antioxidants/metabolism , Antioxidants/pharmacology , Antioxidants/therapeutic use , Disease Management , Humans , Kelch-Like ECH-Associated Protein 1/antagonists & inhibitors , NF-E2-Related Factor 2/agonists , Oxidative Stress/drug effects , Oxidative Stress/physiology
8.
Clin Lab ; 67(12)2021 Dec 01.
Article in English | MEDLINE | ID: covidwho-1551831

ABSTRACT

BACKGROUND: The aim of this study is to investigate the correlation between serum meteorin-like protein levels and thiol/disulfide balance in patients with COVID-19. METHODS: This is a prospective case-control study including 52 PCR-confirmed COVID-19 patients (group 1) and 34 controls (group 2). The present study included patients aged 18 and older who were admitted to the emergency department with symptoms of COVID-19. Meteorin-like protein levels were analyzed using the YL Biont ELISA Kits protocol. Thiol/disulfide balance was studied using the spectrophotometric method. RESULTS: There were 35 males and 17 females in group 1, and 20 males and 14 females in group 2. The groups were similar in terms of gender and age (p > 0.05 and p > 0.05, respectively). Meteorin-like protein was significantly lower in group 1 (p < 0.001). There was no difference between the two groups in terms of total thiol level (p > 0.05). Disulfide, disulfide/native thiol ratio, and disulfide/total thiol ratio were significantly higher in group 1 (p < 0.001, p < 0.001, and p < 0.001, respectively). Native thiol was higher in group 2 (p = 0.002). Native thiol/total thiol ratio was significantly higher in group 2 (p < 0.001). Disulfide, SS/SH%, SS/TT%, and SH/TT% parameters had remarkably high sensitivity (98.1% for them all) and specificity (85.3% for disulfide and 100% for SS/SH%, SS/TT%, and SH/TT%) in differentiating patients and healthy subjects. CONCLUSIONS: In this study, thiol/disulfide balance, which is an indicator of oxidative stress, was disturbed in the disulfide direction and meteorin-like protein was significantly lower in patients with COVID-19. Thiol/disulfide balance and metrnl may play a role in the pathogenesis of COVID-19.


Subject(s)
COVID-19 , Sulfhydryl Compounds , Biomarkers , Case-Control Studies , Female , Homeostasis , Humans , Male , Oxidative Stress , SARS-CoV-2
9.
FASEB J ; 36(1): e22052, 2022 01.
Article in English | MEDLINE | ID: covidwho-1550589

ABSTRACT

The glycocalyx surrounds every eukaryotic cell and is a complex mesh of proteins and carbohydrates. It consists of proteoglycans with glycosaminoglycan side chains, which are highly sulfated under normal physiological conditions. The degree of sulfation and the position of the sulfate groups mainly determine biological function. The intact highly sulfated glycocalyx of the epithelium may repel severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) through electrostatic forces. However, if the glycocalyx is undersulfated and 3-O-sulfotransferase 3B (3OST-3B) is overexpressed, as is the case during chronic inflammatory conditions, SARS-CoV-2 entry may be facilitated by the glycocalyx. The degree of sulfation and position of the sulfate groups will also affect functions such as immune modulation, the inflammatory response, vascular permeability and tone, coagulation, mediation of sheer stress, and protection against oxidative stress. The rate-limiting factor to sulfation is the availability of inorganic sulfate. Various genetic and epigenetic factors will affect sulfur metabolism and inorganic sulfate availability, such as various dietary factors, and exposure to drugs, environmental toxins, and biotoxins, which will deplete inorganic sulfate. The role that undersulfation plays in the various comorbid conditions that predispose to coronavirus disease 2019 (COVID-19), is also considered. The undersulfated glycocalyx may not only increase susceptibility to SARS-CoV-2 infection, but would also result in a hyperinflammatory response, vascular permeability, and shedding of the glycocalyx components, giving rise to a procoagulant and antifibrinolytic state and eventual multiple organ failure. These symptoms relate to a diagnosis of systemic septic shock seen in almost all COVID-19 deaths. The focus of prevention and treatment protocols proposed is the preservation of epithelial and endothelial glycocalyx integrity.


Subject(s)
COVID-19 , Endothelial Cells , Endothelium, Vascular , Glycocalyx , SARS-CoV-2/metabolism , COVID-19/metabolism , COVID-19/pathology , Endothelial Cells/metabolism , Endothelial Cells/pathology , Endothelium, Vascular/metabolism , Endothelium, Vascular/pathology , Glycocalyx/metabolism , Glycocalyx/pathology , Glycocalyx/virology , Humans , Oxidative Stress , Sulfotransferases/metabolism
10.
Nutrients ; 13(12)2021 Nov 28.
Article in English | MEDLINE | ID: covidwho-1542691

ABSTRACT

This article focuses on how nutrition may help prevent and/or assist with recovery from the harmful effects of strenuous acute exercise and physical training (decreased immunity, organ injury, inflammation, oxidative stress, and fatigue), with a focus on nutritional supplements. First, the effects of ketogenic diets on metabolism and inflammation are considered. Second, the effects of various supplements on immune function are discussed, including antioxidant defense modulators (vitamin C, sulforaphane, taheebo), and inflammation reducers (colostrum and hyperimmunized milk). Third, how 3-hydroxy-3-methyl butyrate monohydrate (HMB) may offset muscle damage is reviewed. Fourth and finally, the relationship between exercise, nutrition and COVID-19 infection is briefly mentioned. While additional verification of the safety and efficacy of these supplements is still necessary, current evidence suggests that these supplements have potential applications for health promotion and disease prevention among athletes and more diverse populations.


Subject(s)
Antioxidants/therapeutic use , Athletes , Dietary Supplements , Exercise/immunology , Oxidative Stress , Physical Endurance , COVID-19/epidemiology , COVID-19/immunology , Humans , Inflammation/epidemiology , Inflammation/immunology , Oxidative Stress/drug effects , Oxidative Stress/immunology , Physical Endurance/drug effects , Physical Endurance/immunology , SARS-CoV-2/immunology , Sports Nutritional Sciences
12.
Calcif Tissue Int ; 108(4): 452-460, 2021 04.
Article in English | MEDLINE | ID: covidwho-1509222

ABSTRACT

Bone is not only a mineralized and apparently non-vital structure that provides support for locomotion and protection to inner organs. An increasing number of studies are unveiling new biologic functions and connections to other systems, giving the rise to new fields of research, such as osteoimmunology. The bone marrow niche, a new entity in bone physiology, seems to represent the site where a complex crosstalk between bone and immune/inflammatory responses takes place. An impressive interplay with the immune system is realized in bone marrow, with reciprocal influences between bone cells and haematopoietic cells. In this way, systemic chronic inflammatory diseases realize a crosstalk with bone, resulting in bone disease. Thus, pathogenetic links between chronic kidney disease-mineral bone disorders and osteoporosis, cardiovascular disease, and ageing are common. The aim of this narrative review is to provide a general view of the progresses in the field of bone research and their potential clinical implications, with emphasis on the links with inflammation and the connections to osteoimmunology and chemokines.


Subject(s)
Bone and Bones , Renal Insufficiency, Chronic , Bone Marrow , Humans , Inflammation , Oxidative Stress
13.
Mol Med Rep ; 24(6)2021 Dec.
Article in English | MEDLINE | ID: covidwho-1512771

ABSTRACT

The present study aimed to review major depression, including its types, epidemiology, association with different diseases status and treatments, as well as its correlation with the current COVID-19 pandemic. Mental depression is a common disorder that affects most individuals at one time or another. During depression, there are changes in mood and behavior, accompanied by feelings of defeat, hopelessness, or even suicidal thoughts. Depression has a direct or indirect relation with a number of other diseases including Alzheimer's disease, stroke, epilepsy, diabetes, cardiovascular disease and cancer. In addition, antidepressant drugs have several side effects including sedation, increased weight, indigestion, sexual dysfunction, or a decrease in blood pressure. Stopping medication may cause a relapse of the symptoms of depression and pose a risk of attempted suicide. The pandemic of COVID-19 has affected the mental health of individuals, including patients, individuals contacting patients and medical staff with a number of mental disorders that may adversely affect the immune ability of their bodies. Some of the drugs currently included in the protocols for treating COVID-19 may negatively affect the mental health of patients. Evidence accumulated over the years indicates that serotonin (5HT) deficiencies and norepinephrine (NE) in the brain can lead to mental depression. Drugs that increase levels of NE and 5HT are commonly used in the treatment of depression. The common reason for mood disorders, including mania and bipolar disease are not clearly understood. It is assumed that hyperactivity in specific parts of the brain and excessive activity of neurotransmitters may be involved. Early diagnosis and developing new treatment strategies are essential for the prevention of the severe consequences of depression. In addition, extensive research should be directed towards the investigation of the mental health disturbances occurring during and/or after COVID-19 infection. This may lead to the incorporation of a suitable antidepressant into the current treatment protocols.


Subject(s)
COVID-19/epidemiology , COVID-19/psychology , Depressive Disorder, Major/epidemiology , Antidepressive Agents/adverse effects , Antidepressive Agents/therapeutic use , COVID-19/complications , Cytokine Release Syndrome/etiology , Depressive Disorder, Major/drug therapy , Depressive Disorder, Major/etiology , Depressive Disorder, Major/metabolism , Glutamic Acid/metabolism , Humans , Oxidative Stress
14.
Front Immunol ; 12: 723654, 2021.
Article in English | MEDLINE | ID: covidwho-1504010

ABSTRACT

With the appearance of the SARS-CoV-2 virus in December 2019, all countries in the world have implemented different strategies to prevent its spread and to intensively search for effective treatments. Initially, severe cases of the disease were considered in adult patients; however, cases of older school-age children and adolescents who presented fever, hypotension, severe abdominal pain and cardiac dysfunction, positive for SARS-CoV-2 infection, have been reported, with increased pro-inflammatory cytokines and tissue damage, condition denominated multisystemic inflammatory syndrome (MIS-C); The emerging data from patients with MIS-C have suggested unique characteristics in the immunological response and also clinical similarities with other inflammatory syndromes, which can support as a reference in the search for molecular mechanisms involved in MIS-C. We here in propose that oxidative stress (OE) may play a very important role in the pathophysiology of MIS-C, such as occurs in Kawasaki disease (KD), severe COVID-19 in adults and other processes with characteristics of vascular damage similar to MIS- C, for which we review the available information that can be correlated with possible redox mechanisms.


Subject(s)
COVID-19/complications , Oxidative Stress , SARS-CoV-2/pathogenicity , Systemic Inflammatory Response Syndrome/physiopathology , Adolescent , COVID-19/diagnosis , COVID-19/immunology , COVID-19/physiopathology , Child , Cytokines/immunology , Humans , Inflammation , Systemic Inflammatory Response Syndrome/diagnosis , Systemic Inflammatory Response Syndrome/immunology
15.
Sci Rep ; 11(1): 21633, 2021 11 04.
Article in English | MEDLINE | ID: covidwho-1503836

ABSTRACT

Although the serum lipidome is markedly affected by COVID-19, two unresolved issues remain: how the severity of the disease affects the level and the composition of serum lipids and whether serum lipidome analysis may identify specific lipids impairment linked to the patients' outcome. Sera from 49 COVID-19 patients were analyzed by untargeted lipidomics. Patients were clustered according to: inflammation (C-reactive protein), hypoxia (Horowitz Index), coagulation state (D-dimer), kidney function (creatinine) and age. COVID-19 patients exhibited remarkable and distinctive dyslipidemia for each prognostic factor associated with reduced defense against oxidative stress. When patients were clustered by outcome (7 days), a peculiar lipidome signature was detected with an overall increase of 29 lipid species, including-among others-four ceramide and three sulfatide species, univocally related to this analysis. Considering the lipids that were affected by all the prognostic factors, we found one sphingomyelin related to inflammation and viral infection of the respiratory tract and two sphingomyelins, that are independently related to patients' age, and they appear as candidate biomarkers to monitor disease progression and severity. Although preliminary and needing validation, this report pioneers the translation of lipidome signatures to link the effects of five critical clinical prognostic factors with the patients' outcomes.


Subject(s)
COVID-19/metabolism , Lipids/blood , Serum/chemistry , Adult , Aged , Biomarkers/blood , COVID-19/blood , Dyslipidemias/metabolism , Female , Humans , Italy , Lipidomics/methods , Lipids/analysis , Male , Middle Aged , Oxidative Stress/physiology , Prognosis , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , Sphingomyelins/blood
16.
Food Funct ; 12(20): 9607-9619, 2021 Oct 19.
Article in English | MEDLINE | ID: covidwho-1500759

ABSTRACT

At the end of 2019, the COVID-19 virus spread worldwide, infecting millions of people. Infectious diseases induced by pathogenic microorganisms such as the influenza virus, hepatitis virus, and Mycobacterium tuberculosis are also a major threat to public health. The high mortality caused by infectious pathogenic microorganisms is due to their strong virulence, which leads to the excessive counterattack by the host immune system and severe inflammatory damage of the immune system. This paper reviews the efficacy, mechanism and related immune regulation of epigallocatechin-3-gallate (EGCG) as an anti-pathogenic microorganism drug. EGCG mainly shows both direct and indirect anti-infection effects. EGCG directly inhibits early infection by interfering with the adsorption on host cells, inhibiting virus replication and reducing bacterial biofilm formation and toxin release; EGCG indirectly inhibits infection by regulating immune inflammation and antioxidation. At the same time, we reviewed the bioavailability and safety of EGCG in vivo. At present, the bioavailability of EGCG can be improved to some extent using nanostructured drug delivery systems and molecular modification technology in combination with other drugs. This study provides a theoretical basis for the development of EGCG as an adjuvant drug for anti-pathogenic microorganisms.


Subject(s)
Anti-Infective Agents/pharmacology , Catechin/analogs & derivatives , Catechin/pharmacology , Immunologic Factors/pharmacology , Animals , Antioxidants/pharmacology , COVID-19/drug therapy , Coronavirus/drug effects , Hepatitis Viruses/drug effects , Humans , Inflammation/drug therapy , Mycobacterium tuberculosis/drug effects , Orthomyxoviridae/drug effects , Oxidative Stress/drug effects , SARS-CoV-2/drug effects , Virus Replication/drug effects
17.
Redox Rep ; 26(1): 184-189, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1493448

ABSTRACT

BACKGROUND: COVID-19 is characterized by the presence of oxidative stress. Vitamin D status has been reviewed as one of the factors that may affect disease severity. The aim of this study was to assess the relationship between serum vitamin D levels, oxidative stress markers and disease severity in hospitalized COVID-19 patients. METHODS: Vitamin D levels were measured in 33 patients with COVID-19. The total antioxidant power and plasma peroxides were determined in serum. RESULTS: Severe COVID-19 patients have lower vitamin D levels (18.39 ± 2.29 ng/mL vs. 28.47 ± 3.05 ng/mL, p < .05) and higher oxidative stress compared to the moderate group. When divided according to serum vitamin D levels, significantly higher values of LDH (604.8 ± 76.98 IU/mL vs. 261.57 ± 47.33 IU/mL) and D-dimer (5978 ± 2028ng/mL vs. 977.7 ± 172 ng/mL) were obtained in the group with vitamin D below 30 ng/mL, followed with significantly higher levels of plasma peroxides (d-ROMs: 414.9 ± 15.82 U.Carr vs. 352.4 ± 18.77 U.Carr; p < .05) and oxidative stress index (OSI: 92.25 ± 6.60 vs. 51.89 ± 6.45; p < .001). CONCLUSION: The presented data provide a justification to consider vitamin D as an important factor that could ameliorate disease severity through its anti-inflammatory and antioxidant effects.


Subject(s)
COVID-19/blood , Oxidative Stress , Vitamin D/blood , Adult , Aged , Antioxidants , Biomarkers/blood , COVID-19/diagnosis , Female , Hospitalization , Humans , Male , Middle Aged , Republic of North Macedonia
18.
Sci Rep ; 11(1): 21075, 2021 10 26.
Article in English | MEDLINE | ID: covidwho-1493212

ABSTRACT

Bats are potential natural reservoirs for emerging viruses, causing deadly human diseases, such as COVID-19, MERS, SARS, Nipah, Hendra, and Ebola infections. The fundamental mechanisms by which bats are considered "living bioreactors" for emerging viruses are not fully understood. Some studies suggest that tolerance to viruses is linked to suppressing antiviral immune and inflammatory responses due to DNA damage by energy generated to fly. Our study reveals that bats' gut bacteria could also be involved in the host and its microbiota's DNA damage. We performed screening of lactic acid bacteria and bacilli isolated from bats' feces for mutagenic and oxidative activity by lux-biosensors. The pro-mutagenic activity was determined when expression of recA increased with the appearance of double-strand breaks in the cell DNA, while an increase of katG expression in the presence of hydroxyl radicals indicated antioxidant activity. We identified that most of the isolated bacteria have pro-mutagenic and antioxidant properties at the same time. This study reveals new insights into bat gut microbiota's potential involvement in antiviral response and opens new frontiers in preventing emerging diseases originating from bats.


Subject(s)
Chiroptera/virology , Gastrointestinal Microbiome , Mutagens , Animals , Antioxidants/metabolism , Antiviral Agents , Bacillus , Bacterial Proteins/genetics , Biosensing Techniques , COVID-19 , DNA , DNA Damage , Disease Reservoirs/virology , Escherichia coli/metabolism , Feces , Immune System , Inflammation , Lactic Acid/metabolism , Mass Spectrometry , Mutagenesis , Oxidative Stress , Rec A Recombinases/metabolism , SARS-CoV-2 , Viruses/isolation & purification , Zoonoses/virology
19.
Mech Ageing Dev ; 199: 111551, 2021 10.
Article in English | MEDLINE | ID: covidwho-1492370

ABSTRACT

Polyphenols are chemopreventive through the induction of nuclear factor erythroid 2 related factor 2 (Nrf2)-mediated proteins and anti-inflammatory pathways. These pathways, encoding cytoprotective vitagenes, include heat shock proteins, such as heat shock protein 70 (Hsp70) and heme oxygenase-1 (HO-1), as well as glutathione redox system to protect against cancer initiation and progression. Phytochemicals exhibit biphasic dose responses on cancer cells, activating at low dose, signaling pathways resulting in upregulation of vitagenes, as in the case of the Nrf2 pathway upregulated by hydroxytyrosol (HT) or curcumin and NAD/NADH-sirtuin-1 activated by resveratrol. Here, the importance of vitagenes in redox stress response and autophagy mechanisms, as well as the potential use of dietary antioxidants in the prevention and treatment of multiple types of cancer are discussed. We also discuss the possible relationship between SARS-CoV-2, inflammation and cancer, exploiting innovative therapeutic approaches with HT-rich aqueous olive pulp extract (Hidrox®), a natural polyphenolic formulation, as well as the rationale of Vitamin D supplementation. Finally, we describe innovative approaches with organoids technology to study human carcinogenesis in preclinical models from basic cancer research to clinical practice, suggesting patient-derived organoids as an innovative tool to test drug toxicity and drive personalized therapy.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Antioxidants/pharmacology , Drug Development , NF-E2-Related Factor 2/metabolism , Organoids/drug effects , Oxidative Stress/drug effects , Polyphenols/pharmacology , Vitamin D/pharmacology , Animals , Antineoplastic Agents, Phytogenic/pharmacology , COVID-19/drug therapy , COVID-19/genetics , COVID-19/metabolism , COVID-19/virology , Humans , NF-E2-Related Factor 2/genetics , Neoplasms/drug therapy , Neoplasms/genetics , Neoplasms/metabolism , Neoplasms/pathology , Organoids/metabolism , Oxidation-Reduction , Oxidative Stress/genetics
20.
Oxid Med Cell Longev ; 2021: 5513868, 2021.
Article in English | MEDLINE | ID: covidwho-1467753

ABSTRACT

COVID-19 is a widespread global pandemic with nearly 185 million confirmed cases and about four million deaths. It is caused by an infection with the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which primarily affects the alveolar type II pneumocytes. The infection induces pathological responses including increased inflammation, oxidative stress, and apoptosis. This situation results in impaired gas exchange, hypoxia, and other sequelae that lead to multisystem organ failure and death. As summarized in this article, many interventions and therapeutics have been proposed and investigated to combat the viral infection-induced inflammation and oxidative stress that contributes to the etiology and pathogenesis of COVID-19. However, these methods have not significantly improved treatment outcomes. This may partly be attributable to their inability at restoring redox and inflammatory homeostasis, for which molecular hydrogen (H2), an emerging novel medical gas, may complement. Herein, we systematically review the antioxidative, anti-inflammatory, and antiapoptotic mechanisms of H2. Its small molecular size and nonpolarity allow H2 to rapidly diffuse through cell membranes and penetrate cellular organelles. H2 has been demonstrated to suppress NF-κB inflammatory signaling and induce the Nrf2/Keap1 antioxidant pathway, as well as to improve mitochondrial function and enhance cellular bioenergetics. Many preclinical and clinical studies have demonstrated the beneficial effects of H2 in varying diseases, including COVID-19. However, the exact mechanisms, primary modes of action, and its true clinical effects remain to be delineated and verified. Accordingly, additional mechanistic and clinical research into this novel medical gas to combat COVID-19 complications is warranted.


Subject(s)
COVID-19 , Hydrogen/therapeutic use , Oxidative Stress/drug effects , SARS-CoV-2/metabolism , Signal Transduction/drug effects , COVID-19/drug therapy , COVID-19/metabolism , Humans , Inflammation/drug therapy , Inflammation/metabolism , Kelch-Like ECH-Associated Protein 1/metabolism , NF-E2-Related Factor 2/metabolism , NF-kappa B/metabolism
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