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1.
Br J Pharmacol ; 179(9): 1808-1824, 2022 May.
Article in English | MEDLINE | ID: covidwho-1799274

ABSTRACT

Advancing age is accompanied by significant remodelling of the immune system, termed immune senescence, and increased systemic inflammation, termed inflammageing, both of which contribute towards an increased risk of developing chronic diseases in old age. Age-associated alterations in metabolic homeostasis have been linked with changes in a range of physiological functions, but their effects on immune senescence remains poorly understood. In this article, we review the recent literature to formulate hypotheses as to how an age-associated dysfunctional metabolism, driven by an accumulation of key host metabolites (saturated fatty acids, cholesterol, ceramides and lactate) and loss of other metabolites (glutamine, tryptophan and short-chain fatty acids), might play a role in driving immune senescence and inflammageing, ultimately leading to diseases of old age. We also highlight the potential use of metabolic immunotherapeutic strategies targeting these processes in counteracting immune senescence and restoring immune homeostasis in older adults. LINKED ARTICLES: This article is part of a themed issue on Inflammation, Repair and Ageing. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.9/issuetoc.


Subject(s)
Aging , Immune System , Aged , Cellular Senescence , Homeostasis , Humans , Inflammation
2.
Immunity ; 55(4): 592-605, 2022 Apr 12.
Article in English | MEDLINE | ID: covidwho-1783432

ABSTRACT

Nonresolving inflammation contributes to many diseases, including COVID-19 in its fatal and long forms. Our understanding of inflammation is rapidly evolving. Like the immune system of which it is a part, inflammation can now be seen as an interactive component of a homeostatic network with the endocrine and nervous systems. This review samples emerging insights regarding inflammatory memory, inflammatory aging, inflammatory cell death, inflammatory DNA, inflammation-regulating cells and metabolites, approaches to resolving or modulating inflammation, and inflammatory inequity.


Subject(s)
COVID-19 , Homeostasis , Humans , Immune System/metabolism , Inflammation , Nervous System/metabolism
3.
J Korean Acad Nurs ; 52(1): 36-51, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1742795

ABSTRACT

PURPOSE: The purpose of this study was to examine the effects of electroencephalogram (EEG) biofeedback training for emotion regulation and brain homeostasis on anxiety about COVID-19 infection, impulsivity, anger rumination, meta-mood, and self-regulation ability of late adolescents in the prolonged COVID-19 pandemic situation. METHODS: A non-equivalent control group pretest-posttest design was used. The participants included 55 late adolescents in the experimental and control groups. The variables were evaluated using quantitative EEG at pre-post time points in the experimental group. The experimental groups received 10 sessions using the three-band protocol for five weeks. The collected data were analyzed using the Shapiro-Wilk test, Wilcoxon rank sum test, Wilcoxon signed-rank test, t-test and paired t-test using the SAS 9.3 program. The collected EEG data used a frequency series power spectrum analysis method through fast Fourier transform. RESULTS: Significant differences in emotion regulation between the two groups were observed in the anxiety about COVID-19 infection (W = 585.50, p = .002), mood repair of meta-mood (W = 889.50, p = .024), self-regulation ability (t = -5.02, p < .001), self-regulation mode (t = -4.74, p < .001), and volitional inhibition mode (t = -2.61, p = .012). Neurofeedback training for brain homeostasis was effected on enhanced sensory-motor rhythm (S = 177.00, p < .001) and inhibited theta (S = -166.00, p < .001). CONCLUSION: The results demonstrate the potential of EEG biofeedback training as an independent nursing intervention that can markedly improve anxiety, mood-repair, and self-regulation ability for emotional distress during the COVID-19 pandemic.


Subject(s)
COVID-19 , Emotional Regulation , Neurofeedback , Adolescent , Brain/physiology , Electroencephalography/methods , Homeostasis , Humans , Neurofeedback/methods , Neurofeedback/physiology , Pandemics , SARS-CoV-2
4.
Cells ; 11(6)2022 03 09.
Article in English | MEDLINE | ID: covidwho-1731953

ABSTRACT

The infection with SARS-CoV-2 impairs the glucose-insulin axis and this contributes to oxidative (OS) and nitrosative (NSS) stress. Here, we evaluated changes in glucose metabolism that could promote the loss of redox homeostasis in COVID-19 patients. This was comparative cohort and analytical study that compared COVID-19 patients and healthy subjects. The study population consisted of 61 COVID-19 patients with and without comorbidities and 25 healthy subjects (HS). In all subjects the plasma glucose, insulin, 8-isoprostane, Vitamin D, H2S and 3-nitrotyrosine were determined by ELISA. The nitrites (NO2-), lipid-peroxidation (LPO), total-antioxidant-capacity (TAC), thiols, glutathione (GSH) and selenium (Se) were determined by spectrophotometry. The glucose, insulin and HOMA-IR (p < 0.001), 8-isoprostanes, 3-nitrotyrosine (p < 0.001) and LPO were increased (p = 0.02) while Vitamin D (p = 0.01), H2S, thiols, TAC, GSH and Se (p < 0.001) decreased in COVID-19 patients in comparison to HS. The SARS-CoV-2 infection resulted in alterations in the glucose-insulin axis that led to hyperglycemia, hyperinsulinemia and IR in patients with and without comorbidities. These alterations increase OS and NSS reflected in increases or decreases in some oxidative markers in plasma with major impact or fatal consequences in patients that course with metabolic syndrome. Moreover, subjects without comorbidities could have long-term alterations in the redox homeostasis after infection.


Subject(s)
COVID-19 , Hyperglycemia , Insulin Resistance , Selenium , Antioxidants/metabolism , Glucose , Glutathione/metabolism , Homeostasis , Humans , Hyperglycemia/complications , Insulin/metabolism , Oxidation-Reduction , Oxidative Stress , SARS-CoV-2 , Sulfhydryl Compounds , Vitamin D , Vitamins
5.
Cells ; 11(3)2022 02 04.
Article in English | MEDLINE | ID: covidwho-1674518

ABSTRACT

This review is a comprehensive analysis of the effects of SARS-CoV-2 infection on Unconventional T cells and innate lymphoid cells (ILCs). COVID-19 affected patients show dysregulation of their adaptive immune systems, but many questions remain unsolved on the behavior of Unconventional cells and ILCs during infection, considering their role in maintaining homeostasis in tissue. Therefore, we highlight the differences that exist among the studies in cohorts of patients who in general were categorized considering symptoms and hospitalization. Moreover, we make a critical analysis of the presence of particular clusters of cells that express activation and exhausted markers for each group in order to bring out potential diagnostic factors unconsidered before now. We also focus our attention on studies that take into consideration recovered patients. Indeed, it could be useful to determine Unconventional T cells' and ILCs' frequencies and functions in longitudinal studies because it could represent a way to monitor the immune status of SARS-CoV-2-infected subjects. Possible changes in cell frequencies or activation profiles could be potentially useful as prognostic biomarkers and for future therapy. Currently, there are no efficacious therapies for SARS-CoV-2 infection, but deep studies on involvement of Unconventional T cells and ILCs in the pathogenesis of COVID-19 could be promising for targeted therapies.


Subject(s)
Adaptive Immunity/immunology , COVID-19/immunology , Immunity, Innate/immunology , Lymphocytes/immunology , SARS-CoV-2/immunology , T-Lymphocytes/immunology , COVID-19/epidemiology , COVID-19/virology , Homeostasis/immunology , Humans , Lymphocyte Activation/immunology , Lymphocyte Count , Pandemics/prevention & control , SARS-CoV-2/physiology
6.
Int J Mol Sci ; 23(2)2022 Jan 12.
Article in English | MEDLINE | ID: covidwho-1638520

ABSTRACT

The selenium field expanded at a rapid rate for about 45 years, from the mid-1970's until about 2015 (see [...].


Subject(s)
Disease Susceptibility , Health Impact Assessment , Homeostasis , Selenium/metabolism , Selenoproteins/metabolism , Humans , Selenium/adverse effects
7.
BMC Med ; 20(1): 24, 2022 01 20.
Article in English | MEDLINE | ID: covidwho-1638127

ABSTRACT

BACKGROUND: COVID-19 is an infectious disease characterized by multiple respiratory and extrapulmonary manifestations, including gastrointestinal symptoms. Although recent studies have linked gut microbiota to infectious diseases such as influenza, little is known about the role of the gut microbiota in COVID-19 pathophysiology. METHODS: To better understand the host-gut microbiota interactions in COVID-19, we characterized the gut microbial community and gut barrier function using metagenomic and metaproteomic approaches in 63 COVID-19 patients and 8 non-infected controls. Both immunohematological parameters and transcriptional profiles were measured to reflect the immune response in COVID-19 patients. RESULTS: Altered gut microbial composition was observed in COVID-19 patients, which was characterized by decreased commensal species and increased opportunistic pathogenic species. Severe illness was associated with higher abundance of four microbial species (i.e., Burkholderia contaminans, Bacteroides nordii, Bifidobacterium longum, and Blautia sp. CAG 257), six microbial pathways (e.g., glycolysis and fermentation), and 10 virulence genes. These severity-related microbial features were further associated with host immune response. For example, the abundance of Bu. contaminans was associated with higher levels of inflammation biomarkers and lower levels of immune cells. Furthermore, human-origin proteins identified from both blood and fecal samples suggested gut barrier dysfunction in COVID-19 patients. The circulating levels of lipopolysaccharide-binding protein increased in patients with severe illness and were associated with circulating inflammation biomarkers and immune cells. Besides, proteins of disease-related bacteria (e.g., B. longum) were detectable in blood samples from patients. CONCLUSIONS: Our results suggest that the dysbiosis of the gut microbiome and the dysfunction of the gut barrier might play a role in the pathophysiology of COVID-19 by affecting host immune homeostasis.


Subject(s)
COVID-19 , Gastrointestinal Microbiome , Dysbiosis , Homeostasis , Humans , SARS-CoV-2
8.
Proc Natl Acad Sci U S A ; 119(4)2022 01 25.
Article in English | MEDLINE | ID: covidwho-1621335

ABSTRACT

After binding to its cell surface receptor angiotensin converting enzyme 2 (ACE2), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters the host cell through directly fusing with plasma membrane (cell surface pathway) or undergoing endocytosis traveling to lysosome/late endosome for membrane fusion (endocytic pathway). However, the endocytic entry regulation by host cell remains elusive. Recent studies show ACE2 possesses a type I PDZ binding motif (PBM) through which it could interact with a PDZ domain-containing protein such as sorting nexin 27 (SNX27). In this study, we determined the ACE2-PBM/SNX27-PDZ complex structure, and, through a series of functional analyses, we found SNX27 plays an important role in regulating the homeostasis of ACE2 receptor. More importantly, we demonstrated SNX27, together with retromer complex (the core component of the endosomal protein sorting machinery), prevents ACE2/virus complex from entering lysosome/late endosome, resulting in decreased viral entry in cells where the endocytic pathway dominates. The ACE2/virus retrieval mediated by SNX27-retromer could be considered as a countermeasure against invasion of ACE2 receptor-using SARS coronaviruses.


Subject(s)
Angiotensin-Converting Enzyme 2/metabolism , COVID-19/metabolism , Endosomes/metabolism , SARS-CoV-2 , Sorting Nexins/chemistry , COVID-19/virology , Cell Line , Cell Line, Tumor , Cell Membrane/metabolism , Crystallography, X-Ray , Cytosol/metabolism , Endocytosis , Gene Expression Profiling , HEK293 Cells , HeLa Cells , Homeostasis , Humans , Lentivirus , Lysosomes/metabolism , Peptides/chemistry , Protein Binding , Protein Conformation , Protein Domains , Sorting Nexins/metabolism , Virus Internalization
9.
Microbiol Spectr ; 9(3): e0073521, 2021 12 22.
Article in English | MEDLINE | ID: covidwho-1596765

ABSTRACT

SARS-CoV-2 infection can cause compromised respiratory function and thrombotic events. SARS-CoV-2 binds to and mediates downregulation of angiotensin converting enzyme 2 (ACE2) on cells that it infects. Theoretically, diminished enzymatic activity of ACE2 may result in increased concentrations of pro-inflammatory molecules, angiotensin II, and Bradykinin, contributing to SARS-CoV-2 pathology. Using immunofluorescence microscopy of lung tissues from uninfected, and SARS-CoV-2 infected individuals, we find evidence that ACE2 is highly expressed in human pulmonary alveolar epithelial cells and significantly reduced along the alveolar lining of SARS-CoV-2 infected lungs. Ex vivo analyses of primary human cells, indicated that ACE2 is readily detected in pulmonary alveolar epithelial and aortic endothelial cells. Exposure of these cells to spike protein of SARS-CoV-2 was sufficient to reduce ACE2 expression. Moreover, exposure of endothelial cells to spike protein-induced dysfunction, caspase activation, and apoptosis. Exposure of endothelial cells to bradykinin caused calcium signaling and endothelial dysfunction (increased expression of von Willibrand Factor and decreased expression of Krüppel-like Factor 2) but did not adversely affect viability in primary human aortic endothelial cells. Computer-assisted analyses of molecules with potential to bind bradykinin receptor B2 (BKRB2), suggested a potential role for aspirin as a BK antagonist. When tested in our in vitro model, we found evidence that aspirin can blunt cell signaling and endothelial dysfunction caused by bradykinin in these cells. Interference with interactions of spike protein or bradykinin with endothelial cells may serve as an important strategy to stabilize microvascular homeostasis in COVID-19 disease. IMPORTANCE SARS-CoV-2 causes complex effects on microvascular homeostasis that potentially contribute to organ dysfunction and coagulopathies. SARS-CoV-2 binds to, and causes downregulation of angiotensin converting enzyme 2 (ACE2) on cells that it infects. It is thought that reduced ACE2 enzymatic activity can contribute to inflammation and pathology in the lung. Our studies add to this understanding by providing evidence that spike protein alone can mediate adverse effects on vascular cells. Understanding these mechanisms of pathogenesis may provide rationale for interventions that could limit microvascular events associated with SARS-CoV-2 infection.


Subject(s)
COVID-19/physiopathology , Endothelial Cells/virology , SARS-CoV-2/metabolism , Spike Glycoprotein, Coronavirus/metabolism , Alveolar Epithelial Cells/cytology , Alveolar Epithelial Cells/metabolism , Alveolar Epithelial Cells/virology , Angiotensin-Converting Enzyme 2/chemistry , Angiotensin-Converting Enzyme 2/genetics , Angiotensin-Converting Enzyme 2/metabolism , Aorta/cytology , Aorta/metabolism , Aorta/virology , Apoptosis , Bradykinin/chemistry , Bradykinin/metabolism , COVID-19/genetics , COVID-19/metabolism , COVID-19/virology , Endothelial Cells/cytology , Endothelial Cells/metabolism , Homeostasis , Humans , Lung/blood supply , Lung/metabolism , Lung/virology , Microcirculation , Receptors, Bradykinin/chemistry , Receptors, Bradykinin/genetics , Receptors, Bradykinin/metabolism , SARS-CoV-2/genetics , Spike Glycoprotein, Coronavirus/chemistry , Spike Glycoprotein, Coronavirus/genetics
10.
Front Immunol ; 12: 762782, 2021.
Article in English | MEDLINE | ID: covidwho-1593084

ABSTRACT

Coagulopathy is a frequently reported finding in the pathology of coronavirus disease 2019 (COVID-19); however, the molecular mechanism, the involved coagulation factors, and the role of regulatory proteins in homeostasis are not fully investigated. We explored the dynamic changes of nine coagulation tests in patients and controls to propose a molecular mechanism for COVID-19-associated coagulopathy. Coagulation tests including prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen (FIB), lupus anticoagulant (LAC), proteins C and S, antithrombin III (ATIII), D-dimer, and fibrin degradation products (FDPs) were performed on plasma collected from 105 individuals (35 critical patients, 35 severe patients, and 35 healthy controls). There was a statically significant difference when the results of the critical (CRT) and/or severe (SVR) group for the following tests were compared to the control (CRL) group: PTCRT (15.014) and PTSVR (13.846) (PTCRL = 13.383, p < 0.001), PTTCRT (42.923) and PTTSVR (37.8) (PTTCRL = 36.494, p < 0.001), LACCRT (49.414) and LACSVR (47.046) (LACCRL = 40.763, p < 0.001), FIBCRT (537.66) and FIBSVR (480.29) (FIBCRL = 283.57, p < 0.001), ProCCRT (85.57%) and ProCSVR (99.34%) (ProCCRL = 94.31%, p = 0.04), ProSCRT (62.91%) and ProSSVR (65.06%) (ProSCRL = 75.03%, p < 0.001), D-dimer (p < 0.0001, χ 2 = 34.812), and FDP (p < 0.002, χ 2 = 15.205). No significant association was found in the ATIII results in groups (ATIIICRT = 95.71% and ATIIISVR = 99.63%; ATIIICRL = 98.74%, p = 0.321). D-dimer, FIB, PT, PTT, LAC, protein S, FDP, and protein C (ordered according to p-values) have significance in the prognosis of patients. Disruptions in homeostasis in protein C (and S), VIII/VIIIa and V/Va axes, probably play a role in COVID-19-associated coagulopathy.


Subject(s)
Blood Coagulation Disorders/blood , Blood Coagulation Tests/methods , Blood Coagulation , COVID-19/complications , Adult , Aged , Blood Coagulation Disorders/complications , Blood Coagulation Disorders/diagnosis , Blood Coagulation Factors/metabolism , COVID-19/virology , Female , Fibrin/metabolism , Fibrin Fibrinogen Degradation Products/metabolism , Homeostasis , Humans , Male , Middle Aged , Partial Thromboplastin Time , Prognosis , Protein C/metabolism , Prothrombin Time , SARS-CoV-2/genetics , SARS-CoV-2/physiology
11.
Viruses ; 13(12)2021 11 25.
Article in English | MEDLINE | ID: covidwho-1590034

ABSTRACT

Disease tolerance has emerged as an alternative way, in addition to host resistance, to survive viral-bacterial co-infections. Disease tolerance plays an important role not in reducing pathogen burden, but in maintaining tissue integrity and controlling organ damage. A common co-infection is the synergy observed between influenza virus and Streptococcus pneumoniae that results in superinfection and lethality. Several host cytokines and cells have shown promise in promoting tissue protection and damage control while others induce severe immunopathology leading to high levels of morbidity and mortality. The focus of this review is to describe the host cytokines and innate immune cells that mediate disease tolerance and lead to a return to host homeostasis and ultimately, survival during viral-bacterial co-infection.


Subject(s)
Immunity, Innate , Influenza, Human/immunology , Orthomyxoviridae/immunology , Pneumococcal Infections/immunology , Streptococcus pneumoniae/immunology , Coinfection , Cytokines/immunology , Homeostasis , Humans , Influenza, Human/microbiology , Influenza, Human/virology , Pneumococcal Infections/microbiology , Superinfection
12.
BMC Gastroenterol ; 21(1): 462, 2021 Dec 11.
Article in English | MEDLINE | ID: covidwho-1571741

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is defined as an emerging infectious disease caused by severe acute respiratory syndrome coronavirus 2 and celiac disease (CD) is one of the autoimmune multiorgan diseases, which can be accompanied by an increased risk of viral infections. CD patients, especially untreated subjects, may be at greater risk of infections such as viral illnesses. Interleukin (IL)-6, CD4, CD25, and FOXP3 are known as genes affecting immune homeostasis and relate to the inflammation state. This study aimed to compare the expression levels of aforementioned genes in peripheral blood samples of CD and severe COVID-19 patients. METHODS: Sixty newly diagnosed CD patients with median age (mean ± SD) of 35.40 ± 24.12 years; thirty confirmed severe COVID-19 patients with median age (mean ± SD) of 59.67 ± 17.22, and 60 healthy subjects with median age (mean ± SD) of 35.6 ± 13.02 years; were recruited from March to September 2020. Fresh whole blood samples were collected, total RNA was obtained and cDNA synthesis was carried out. RNA expression levels of IL-6, CD4, CD25, and FOXP3 genes were assessed using real-time quantitative RT-PCR according to the 2-∆∆Ct formula. Statistical analysis was performed using SPSS (V.21) and GraphPad, Prism (V.6). RESULTS: While increased expression of CD4, CD25, and FOXP3 was observed in CD patients compared to the control group (p = 0.02, p = 0.03, and p < 0.0001 respectively) and COVID-19 patients group (p < 0.0001 for all of them), their expression levels in COVID-19 patients decreased compared to controls (p < 0.0001, p = 0.01, p = 0.007, respectively). Increased IL-6 expression was observed in both groups of patients compared to controls (p < 0.0001 for both of them). CONCLUSIONS: Although untreated CD patients may be at greater risk of developing into severe COVID-19 if they are infected by SARS-CoV-2 virus (due to their high expression of IL-6), increased expression of anti-inflammatory markers in these patients may be beneficial for them with the ability of reducing the severity of COVID-19 disease, which needs to be proven in future studies involving celiac patients infected with COVID-19.


Subject(s)
COVID-19 , Celiac Disease , Adolescent , Adult , Celiac Disease/genetics , Child , Forkhead Transcription Factors/genetics , Homeostasis , Humans , Interleukin-2 , Interleukin-6/genetics , Middle Aged , SARS-CoV-2 , T-Lymphocytes, Regulatory , Young Adult
13.
J Inorg Biochem ; 228: 111691, 2022 03.
Article in English | MEDLINE | ID: covidwho-1558451

ABSTRACT

Zinc can play a pathophysiological role in several diseases and can interfere in key processes of microbial growth. This evidence justifies the efforts in applying Zinc ionophores to restore Zinc homeostasis and treat bacterial/viral infections such as coronavirus diseases. Zinc ionophores increase the intracellular concentration of Zinc ions causing significant biological effects. This review provides, for the first time, an overview of the applications of the main Zinc ionophores in Zinc deficiency, infectious diseases, and in cancer, discussing the pharmacological and coordination properties of the Zinc ionophores.


Subject(s)
Communicable Diseases/drug therapy , Ionophores/chemistry , Neoplasms/drug therapy , Zinc/chemistry , Zinc/pharmacology , Acrodermatitis/drug therapy , Anti-Bacterial Agents/pharmacology , Antineoplastic Agents/pharmacology , Antiviral Agents/pharmacology , COVID-19/drug therapy , Homeostasis/drug effects , Humans , Ionophores/pharmacology , Zinc/deficiency
14.
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
15.
Front Biosci (Landmark Ed) ; 26(11): 1132-1146, 2021 11 30.
Article in English | MEDLINE | ID: covidwho-1552202

ABSTRACT

Background: COVID-19 pandemic has exacerbated the problem of physical inactivity and weight gain. Consequently, new strategies to counteract weight gain are being sought. Because of their accessibility, interval training and cold therapy are the most popular such strategies. We here aimed to examine the effect of 6 units of high-intensity interval training (HIIT), applied alone or in combination with 10 sessions of whole-body cryotherapy (WBC; 3 min at -110 ∘C per session) on incretins, myokines, and adipokines levels. Materials and methods: The study involved 65 subjects (body mass index of approximately 30 kg•m-2). The subjects were randomly divided into training group (TR; n = 27) and training supported by WBC group (TR-WBC; n = 38). Blood samples were collected before, immediately following, and 4 weeks after the intervention. Results: Fibroblast growth factor 21 (FGF21) levels significantly increased (p = 0.03) and adiponectin levels increased in the TR group (p = 0.05) compared with those recorded in TR-WBC group 24 h after the end of experimental protocol. Beneficial changes in the lipid profile (p = 0.07), a significant drop in visfatin levels (p < 0.05), and the improvement in ß-cell function (HOMA-B; p = 0.02) were also observed in the TR group in the same time point of study. While TR-WBC did not induce similar changes, it ameliorated blood glucose levels (p = 0.03). Changes induced by both interventions were only sustained for 4 weeks after treatment. Conclusion: Collectively, HIIT, alone and in combination with WBC, positively affects metabolic indicators, albeit, most likely, different mechanisms drive the beneficial effects of different treatments.


Subject(s)
Adipokines/metabolism , Cryotherapy , Cytokines/metabolism , Glucose/metabolism , High-Intensity Interval Training , Homeostasis , Obesity/physiopathology , Overweight/physiopathology , Humans , Obesity/metabolism , Overweight/metabolism
16.
Eur J Nutr ; 61(2): 625-636, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1482208

ABSTRACT

PURPOSE: In less than one and a half year, the COVID-19 pandemic has nearly brought to a collapse our health care and economic systems. The scientific research community has concentrated all possible efforts to understand the pathogenesis of this complex disease, and several groups have recently emphasized recommendations for nutritional support in COVID-19 patients. In this scoping review, we aim at encouraging a deeper appreciation of magnesium in clinical nutrition, in view of the vital role of magnesium and the numerous links between the pathophysiology of SARS-CoV-2 infection and magnesium-dependent functions. METHODS: By searching PubMed and Google Scholar from 1990 to date, we review existing evidence from experimental and clinical studies on the role of magnesium in chronic non-communicable diseases and infectious diseases, and we focus on recent reports of alterations of magnesium homeostasis in COVID-19 patients and their association with disease outcomes. Importantly, we conduct a census on ongoing clinical trials specifically dedicated to disclosing the role of magnesium in COVID-19. RESULTS: Despite many methodological limitations, existing data seem to corroborate an association between deranged magnesium homeostasis and COVID-19, and call for further and better studies to explore the prophylactic or therapeutic potential of magnesium supplementation. CONCLUSION: We propose to reconsider the relevance of magnesium, frequently overlooked in clinical practice. Therefore, magnesemia should be monitored and, in case of imbalanced magnesium homeostasis, an appropriate nutritional regimen or supplementation might contribute to protect against SARS-CoV-2 infection, reduce severity of COVID-19 symptoms and facilitate the recovery after the acute phase.


Subject(s)
COVID-19 , Homeostasis , Humans , Magnesium , Pandemics , SARS-CoV-2
17.
Cells ; 10(9)2021 09 13.
Article in English | MEDLINE | ID: covidwho-1468387

ABSTRACT

Neutrophils are key cells of the innate immune system. It is now understood that this leukocyte population is diverse in both the basal composition and functional plasticity. Underlying this plasticity is a post-translational framework for rapidly achieving early activation states, but also a transcriptional capacity that is becoming increasingly recognized by immunologists. Growing interest in the contribution of neutrophils to health and disease has resulted in more efforts to describe their transcriptional activity. Whilst initial efforts focused predominantly on understanding the existing biology, investigations with advanced methods such as single cell RNA sequencing to understand interactions of the entire immune system are revealing higher flexibility in neutrophil transcription than previously thought possible and multiple transition states. It is now apparent that neutrophils utilise many forms of RNA in the regulation of their function. This review collates current knowledge on the nuclei structure and gene expression activity of human neutrophils across homeostasis and disease, before highlighting knowledge gaps that are research priority areas.


Subject(s)
Disease/etiology , Gene Expression Regulation , Immunity, Innate/immunology , Neutrophils/immunology , Neutrophils/pathology , Transcriptome , Animals , Homeostasis , Humans , Neutrophils/metabolism , Signal Transduction
18.
Front Immunol ; 12: 753940, 2021.
Article in English | MEDLINE | ID: covidwho-1463477

ABSTRACT

Lung macrophages play important roles in the maintenance of homeostasis, pathogen clearance and immune regulation. The different types of pulmonary macrophages and their roles in lung diseases have attracted attention in recent years. Alveolar macrophages (AMs), including tissue-resident alveolar macrophages (TR-AMs) and monocyte-derived alveolar macrophages (Mo-AMs), as well as interstitial macrophages (IMs) are the major macrophage populations in the lung and have unique characteristics in both steady-state conditions and disease states. The different characteristics of these three types of macrophages determine the different roles they play in the development of disease. Therefore, it is important to fully understand the similarities and differences among these three types of macrophages for the study of lung diseases. In this review, we will discuss the physiological characteristics and unique functions of these three types of macrophages in acute and chronic lung diseases. We will also discuss possible methods to target macrophages in lung diseases.


Subject(s)
COVID-19/immunology , Lung Diseases/immunology , Lung/immunology , Macrophages/immunology , SARS-CoV-2/physiology , Animals , Homeostasis , Humans , Inflammation
19.
Mycopathologia ; 186(6): 877-882, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1460405

ABSTRACT

Mucorales is the cause of mucormycosis, an emerging opportunistic infection in the era of coronavirus disease 2019 (COVID-19) pandemic. Condition of hyperglycemia, diabetes mellitus, and acidosis; dysregulated iron homeostasis in the form of hyperferritinemic syndrome, and high concentration of iron in circulation; and endothelial injury related to abundance glucose regulated protein 78 (GRP78), which are present in severe COVID-19, could favor Mucorales infection. In this short communication, we summarized how the dysregulated iron homeostasis in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection benefits Mucorales.


Subject(s)
COVID-19 , Mucorales , Mucormycosis , Homeostasis , Humans , Iron , SARS-CoV-2
20.
Physiology (Bethesda) ; 35(6): 361-362, 2020 11 01.
Article in English | MEDLINE | ID: covidwho-1443664
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