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1.
Kidney Int ; 2022 Nov 09.
Article in English | MEDLINE | ID: covidwho-2105523

ABSTRACT

The most common cause of acute kidney injury (AKI) in critically ill patients is sepsis. Kidney macrophages consist of both F4/80hi and CD11bhi cells. The role of macrophage subpopulations in septic AKI pathogenesis remains unclear. As F4/80hi macrophages are reported to contribute to immunomodulation following injury, we hypothesized that selective depletion of F4/80hi macrophages would worsen septic AKI. F4/80hi macrophages were depleted via diphtheria toxin injection in CD11cCre(+)/CX3CR1dtr/wt (F4/80 MKO mice) compared to CD11cCre(-)/CX3CR1dtr/wt (F4/80 MWT) mice. F4/80 MWT and F4/80 MKO mice were subjected to sham or cecal ligation and puncture to induce sepsis. Compared to F4/80 MWT mice, F4/80 MKO mice displayed worsened septic AKI at 24 hours as measured by serum creatinine and histologic injury scoring. Kidneys from F4/80 MKO mice elaborated higher kidney interleukin-6 levels. Mechanistically, single cell RNA sequencing identified a macrophage-endothelial cell immunoregulatory axis that underlies interleukin-6 expression. F4/80hi macrophages expressed interleukin-1 receptor antagonist and limited interleukin-6 expression in endothelial cells. In turn, anti-interleukin-6 therapy ameliorated septic AKI in F4/80 MKO mice. Thus, F4/80hi macrophages express interleukin-1 receptor antagonist and constrain interleukin-6 generation from endothelial cells to limit septic AKI, representing a targetable cellular crosstalk in septic AKI. These findings are particularly relevant owing to the efficacy of anti-interleukin-6 therapies during COVID-19 infection, a disease associated with high rates of AKI and endothelial dysfunction.

2.
Nephrology and Dialysis ; JOUR(2):279-291, 24.
Article in Russian | Scopus | ID: covidwho-2100887

ABSTRACT

Cytokine release syndrome plays a key role in the pathogenesis of COVID-19. Therapeutic plasma exchange (TPE) by removing pathogenic cytokines, can favorably influence the course of severe forms of this disease. However, conclusive studies on this issue are still lacking. Only descriptions of individual clinical cases or small cohort studies have been published. There are no data on the use of TPE in patients with renal failure in the literature. The study aims to evaluate the effect of TPE in the severe forms of COVID-19 in patients with advanced renal failure. Material and Methods: a retrospective, uncontrolled, observational study enrolled 211 patients aged 60,4±13,2. 90.5% of them received renal replacement therapy: 66.8% – hemodialysis, 9.5% – peritoneal dialysis, 14.2% renal transplant recipients with moderate to severe dysfunction, and 9.5% had acute kidney injury on chronic kidney disease that did not require dialysis treatment. Results. All patients were divided into 2 groups: 124 (58.8%) patients (treated from 01.07. to 15.12.2020), who received TPE (TPE group), and 87 (41.2%) patients (observed from 01.04. to 30.06.2020), who did not treat with TPE (control group). The condition of patients in both groups at admission was approximately comparable. The clinical picture of the disease was dominated by severe pneumonia. There were no significant differences in inflammatory markers: both groups had no significant differences in levels of CRP, ferritin, lactate dehydrogenase, or D-dimer. The groups also did not differ significantly in lymphopenia, thrombocytopenia, and azotemia. The mortality rate in the group of patients who did not receive TPE was 73.5%, while in the TPE group it was 45.16% (p<0.001). Among patients on chronic dialysis, the mortality rate in the control subgroup was 74.6%, and in the TPE subgroup – 44.15% (p<0.001). Conclusion:therapeutic plasma exchange is an efficient approach to the treatment of severe forms of COVID-19 in patients with advanced renal failure. Its effect, however, may be limited by the risk of death due to uremia. © 2022 JSC Vidal Rus. All rights reserved.

3.
Int J Mol Sci ; 23(21)2022 Nov 07.
Article in English | MEDLINE | ID: covidwho-2099582

ABSTRACT

Autoimmune thyroid diseases (AITDs), which include Hashimoto's thyroiditis (HT) and Graves' disease (GD), have a higher prevalence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in the literature. The effects of AITD-associated cytokines on SARS-CoV-2 infection-mediating molecule levels might be involved in the pathogenesis of susceptibility. We speculated that hydrogen sulfide (H2S) might attenuate this process since H2S has antiviral effects. Using immunohistochemistry, we found that angiotensin-converting enzyme-II (ACE2) expression was higher in the HT group and neuropilin 1 (NRP1) expression was higher in HT and GD groups than in the normal group, while transmembrane protease serine type 2 (TMPRSS2) expression was lower in HT and GD groups. When culturing primary thyrocytes with cytokines or sodium hydrosulfide (NaHS) plus cytokines, we found that ACE2 and NRP1 mRNA levels were upregulated while TMPRSS2 levels were downregulated by interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α). After pretreatment with NaHS in thyrocytes, ACE2 and NRP1 expression were downregulated compared to IFN-γ or TNF-α treatment, and NaHS had no effect on TMPRSS2 expression. Our findings suggested that IFN-γ and TNF-α, which are elevated in AITDs, promoted ACE2 and NRP1 expression and inhibited TMPRSS2 expression. H2S might protect against SARS-CoV-2 infection by downregulating ACE2 and NRP1 levels.


Subject(s)
COVID-19 , Graves Disease , Hydrogen Sulfide , Humans , SARS-CoV-2 , Tumor Necrosis Factor-alpha/pharmacology , Interferon-gamma/pharmacology , Angiotensin-Converting Enzyme 2/genetics , Hydrogen Sulfide/pharmacology , Peptidyl-Dipeptidase A/metabolism
4.
Transl Med Commun ; 7(1): 3, 2022.
Article in English | MEDLINE | ID: covidwho-2098471

ABSTRACT

Background: Dysregulation of antiviral immunity has been implicated in the progression of acute respiratory syndrome coronavirus 2 infection into severe cases of coronavirus disease of 2019 (COVID-19). Imbalances in the inflammatory response drive the overabundant production of pro-inflammatory cytokines and chemokines. The low molecular weight fraction of 5% human serum albumin commercial preparation (AMP5A) is a novel biologic drug currently under clinical investigation for the treatment of osteoarthritis and the hyperinflammatory response associated with COVID-19. This study aims to elucidate AMP5A effects following the activation of immune cells with agonists of Toll-like receptor (TLR) 7 and/or 8, which detect ssRNA viral sequences. Methods: CXCL10 ELISAs were used to evaluate the dynamics of myeloid cells activated with CL075 and CL307, agonists of TLR7/8 and TLR7, respectively. In addition, enrichment analysis of gene sets generated by ELISA arrays was utilized to gain insight into the biologic processes underlying the identified differentially expressed cytokine profiles. Finally, relative potency (REP) was employed to confirm the involvement of mechanisms of action paramount to AMP5A activity. Results: AMP5A inhibits the release of CXCL10 from both CL075- and CL307-activated PMA-differentiated THP-1 and peripheral blood mononuclear cells. Furthermore, AMP5A suppresses a distinct set of pro-inflammatory cytokines (including IL-1ß, IL-6, IL-12, and CXCL10) associated with COVID-19 and pro-inflammatory NF-κB activation. REP experiments using antagonists specific for the immunomodulatory transcription factors, peroxisome proliferator-activated receptor γ, and aryl hydrocarbon receptor, also indicate that these pathways are involved in the ability of AMP5A to inhibit CXCL10 release. Conclusion: Due to the biphasic course of COVID-19, therapeutic approaches that augment antiviral immunity may be more beneficial early in infection, whereas later interventions should focus on inflammation suppression. In this study, we show that AMP5A inhibits TLR 7/8 signaling in myeloid cells, resulting in a decrease in inflammatory mediators associated with hyperinflammation and autoimmunity. Furthermore, data demonstrating that AMP5A activates immunomodulatory transcription factors found to be protective in lung disease is provided. These findings suggest that the modes and mechanisms of action of AMP5A are well suited to treat conditions involving dysregulated TLR 7/8 activation.

5.
Ter Arkh ; 94(5): 605-609, 2022 Jun 17.
Article in Russian | MEDLINE | ID: covidwho-2091498

ABSTRACT

Despite great advances in the diagnosis and treatment of immunoinflammatory rheumatic diseases, which have led to a significant improvement in the prognosis in many patients, the fundamental medical problems of this pathology the restoration of the quality of life and the reduction of mortality to the population level are far from being resolved. This served as a stimulus for the study of new approaches to the pharmacotherapy of IVRD, one of which is associated with the use of low molecular weight chemically synthesized drugs that inhibit intracellular "signaling" molecules Janus kinase. Modern advances regarding the use of Janus kinase inhibitors in the treatment of immunoinflammatory rheumatic diseases and COVID -19 are considered.


Subject(s)
COVID-19 , Janus Kinase Inhibitors , Rheumatic Diseases , Synthetic Drugs , Humans , Janus Kinase Inhibitors/adverse effects , Quality of Life , COVID-19/drug therapy , Rheumatic Diseases/drug therapy , Janus Kinases/therapeutic use , Synthetic Drugs/therapeutic use
6.
Rev Invest Clin ; 2022 Oct 25.
Article in English | MEDLINE | ID: covidwho-2091423

ABSTRACT

Initial reports suggested that kidney involvement after coronavirus disease 19 (COVID-19) infection was uncommon, but this premise appears to be incorrect. Acute kidney injury can occur through various mechanisms and complicate the course of up to 25% of patients with COVID-19 hospitalized in our Institution, and of over 50% of those on invasive mechanical ventilation. Mechanisms of injury include direct kidney injury and predominantly tubular, although glomerular injury has been reported, and resulting from severe hypoxic respiratory failure, secondary infection, and exposure to nephrotoxic drugs. The mainstay of treatment remains the prevention of progressive kidney damage and, in some cases, the use of renal replacement therapy. Although the use of blood purification techniques has been proposed as a potential treatment, results to date have not been conclusive. In this manuscript, the mechanisms of kidney injury by COVID-19, risk factors, and the mainstays of treatment are reviewed.

7.
J Clin Invest ; 2022 Oct 25.
Article in English | MEDLINE | ID: covidwho-2089017

ABSTRACT

BACKGROUND: Heterologous effects of vaccines are mediated by 'trained immunity' whereby myeloid cells are metabolically and epigenetically reprogrammed resulting in heightened responses to subsequent insults. Adenovirus vaccine vector has been reported to induce trained immunity in mice. Therefore, we sought to determine if the ChAdOx1 nCoV-19 vaccine (AZD1222), which uses an adenoviral vector, could induce trained immunity in vivo in humans. METHODS: Ten healthy volunteers donated blood on the day before receiving the ChAdOx1 nCoV-19 vaccine and on day 14, 56 and 90 post vaccination. Monocytes were purified from PBMC; cell phenotype was determined by flow cytometry, expression of metabolic enzymes were quantified by RT-qPCR and production of cytokines and chemokine in response to stimulation ex vivo were analyzed by multiplex ELISA. RESULTS: Monocyte frequency and count were increased in peripheral blood up to 3 months post vaccination compared with their own pre-vaccine control. Expression of HLA-DR, CD40 and CD80 was enhanced on monocytes for up to 3 months following vaccination. Moreover, monocytes had increased expression of glycolysis-associated enzymes 2 months post vaccination. Upon stimulation ex vivo with unrelated antigens, monocytes produced increased IL-1ß, IL-6, IL-10, CXCL1, and MIP-1α, and decreased TNF, compared with pre-vaccine controls. Resting monocytes produced more IFN-γ, IL-18, and MCP-1 up to 3 months post vaccination compared with pre-vaccine controls. CONCLUSION: These data provide evidence for the induction of trained immunity following a single dose of the ChAdOx1 nCoV-19 vaccine. FUNDING: This work was funded by The Health Research Board (EIA-2019-010) and Science Foundation Ireland Strategic Partnership Programme (Proposal ID 20/SPP/3685).

8.
Brief Funct Genomics ; 21(6): 423-432, 2022 Nov 17.
Article in English | MEDLINE | ID: covidwho-2087742

ABSTRACT

The elevated levels of inflammatory cytokines have attracted much attention during the treatment of COVID-19 patients. The conclusions of current observational studies are often controversial in terms of the causal effects of COVID-19 on various cytokines because of the confounding factors involving underlying diseases. To resolve this problem, we conducted a Mendelian randomization analysis by integrating the GWAS data of COVID-19 and 41 cytokines. As a result, the levels of 2 cytokines were identified to be promoted by COVID-19 and had unsignificant pleiotropy. In comparison, the levels of 10 cytokines were found to be inhibited and had unsignificant pleiotropy. Among down-regulated cytokines, CCL2, CCL3 and CCL7 were members of CC chemokine family. We then explored the potential molecular mechanism for a significant causal association at a single cell resolution based on single-cell RNA data, and discovered the suppression of CCL3 and the inhibition of CCL3-CCR1 interaction in classical monocytes (CMs) of COVID-19 patients. Our findings may indicate that the capability of COVID-19 in decreasing the chemotaxis of lymphocytes by inhibiting the CCL3-CCR1 interaction in CMs.

9.
Eur J Immunol ; 2022 Oct 22.
Article in English | MEDLINE | ID: covidwho-2085026

ABSTRACT

After recovery, mild and severe COVID-19 diseases are associated with long-term effects on the host immune system, such as prolonged T-cell activation or accumulation of autoantibodies. In this study, we show that mild SARS-CoV-2 infections, but not SARS-CoV-2 spike mRNA vaccinations, cause durable atopic risk factors such as a systemic Th2- and Th17-type environment as well as activation of B cells responsive of IgE against aeroallergens from house dust mite and mold. At an average of 100 days post mild SARS-CoV-2 infections, anti-mold responses were associated with low IL-13 levels and increased pro-inflammatory IL-6 titers. Acutely severely ill COVID-19 patients instead showed no evidence of atopic reactions. Considering convalescents of mild COVID-19 courses and mRNA-vaccinated individuals together, IL-13 was the predominant significantly upregulated factor, likely shaping SARS-CoV-2 immunity. Application of multiple regression analysis revealed that the IL-13 levels of both groups were determined by the Th17-type cytokines IL-17A and IL-22. Taken together, these results implicate a critical role for IL-13 in the aftermath of SARS-CoV-2 mild infections and mRNA vaccinations, conferring protection against airway directed, atopic side reactions that occur in mildly experienced COVID-19.

10.
European Review for Medical and Pharmacological Sciences ; JOUR(15):5596-5600, 26.
Article in English | Web of Science | ID: covidwho-2081693

ABSTRACT

- OBJECTIVE: SARS-CoV-2 infection is associated with a higher risk of acute right heart failure (RHF) due to primary right ventricle (RV) dilation and systemic inflammatory response, which in turn lead to microvascular and cardiomyocytes dysfunction, local hypoxia and multi-organ failure. In this clinical setting, levosimendan could be a viable therapy thanks to its right-heart tropism and its additional pleiotropic properties. CASE REPORT: We present the case of a 72 years-old man with positive nasopharyngeal swab for SARS-CoV-2 infection, mild pulmonary involvement and clinical signs of new-onset RHF. We started a 12-hour levosimendan cycle to improve RV performance and reduce cardiac filling pressures. RESULTS: We obtained a net clinical benefit in terms of acute RHF-related signs and symptoms, progressive renal and liver function improvement and concomitant reduction of high-sensitivity C-Reactive Protein and Interleukin-6 (IL-6) levels. CONCLUSIONS: Acute RHF during SARSCoV-2 infection could be related to a convergent widespread systemic inflammatory response. Thanks to its anti-inflammatory and anti-remodsponse.

11.
Int J Mol Sci ; 23(21)2022 Oct 22.
Article in English | MEDLINE | ID: covidwho-2081827

ABSTRACT

Systemic juvenile idiopathic arthritis (sJIA) and its complication, macrophage activation syndrome (sJIA-MAS), are rare but sometimes very serious or even critical diseases of childhood that can occasionally be characterized by nonspecific clinical signs and symptoms at onset-such as non-remitting high fever, headache, rash, or arthralgia-and are biologically accompanied by an increase in acute-phase reactants. For a correct positive diagnosis, it is necessary to rule out bacterial or viral infections, neoplasia, and other immune-mediated inflammatory diseases. Delays in diagnosis will result in late initiation of targeted therapy. A set of biomarkers is useful to distinguish sJIA or sJIA-MAS from similar clinical entities, especially when arthritis is absent. Biomarkers should be accessible to many patients, with convenient production and acquisition prices for pediatric medical laboratories, as well as being easy to determine, having high sensitivity and specificity, and correlating with pathophysiological disease pathways. The aim of this review was to identify the newest and most powerful biomarkers and their synergistic interaction for easy and accurate recognition of sJIA and sJIA-MAS, so as to immediately guide clinicians in correct diagnosis and in predicting disease outcomes, the response to treatment, and the risk of relapses. Biomarkers constitute an exciting field of research, especially due to the heterogeneous nature of cytokine storm syndromes (CSSs) in the COVID era. They must be selected with utmost care-a fact supported by the increasingly improved genetic and pathophysiological comprehension of sJIA, but also of CSS-so that new classification systems may soon be developed to define homogeneous groups of patients, although each with a distinct disease.


Subject(s)
Arthritis, Juvenile , COVID-19 , Macrophage Activation Syndrome , Humans , Child , Macrophage Activation Syndrome/diagnosis , Macrophage Activation Syndrome/drug therapy , Macrophage Activation Syndrome/etiology , Arthritis, Juvenile/diagnosis , Arthritis, Juvenile/drug therapy , COVID-19/diagnosis , Biomarkers
12.
Front Immunol ; 13: 985433, 2022.
Article in English | MEDLINE | ID: covidwho-2080149

ABSTRACT

Multisystem inflammatory syndrome in children (MIS-C) is a rare, severe complication of COVID-19. A better knowledge of immunological, cellular, and genetic characteristics of MIS-C could help better understand the pathogenesis of the disease and contribute to identifying specific diagnostic biomarkers and develop targeted therapies. We studied 37 MIS-C children at hospital admission and 24 healthy controls analyzing serum cytokines (IFN-α, IFN-ß, IFN-γ, IL-6, IL-10, IL-17A, IL-12p70 and TNF), lymphocyte populations by flow cytometry and 386 genes related to autoimmune diseases, autoinflammation and primary immunodeficiencies by NGS. MIS-C patients showed a significant increase of serum IFNγ (despite a significant reduction of activated Th1) and ILs, even if with a great heterogeneity among patients, revealing different pathways involved in MIS-C pathogenesis and suggesting that serum cytokines at admission may help to select the inflammatory pathways to target in each patient. Flow cytometry demonstrated a relevant reduction of T populations while the percentage of B cell was increased in agreement with an autoimmune pathogenesis of MIS-C. Genetic analysis identified variants in 34 genes and 83.3% of patients had at least one gene variant. Among these, 9 were mutated in more patients. Most genes are related to autoimmune diseases like ATM, NCF1, MCM4, FCN3, and DOCK8 or to autoinflammatory diseases associated to the release of IFNγ like PRF1, NOD2, and MEF. Thus, an incomplete clearance of the Sars-CoV2 during the acute phase may induce tissue damage and self-antigen exposure and genetic variants can predispose to hyper-reactive immune dysregulation events of MIS-C-syndrome. Type II IFN activation and cytokine responses (mainly IL-6 and IL-10) may cause a cytokine storm in some patients with a more severe acute phase of the disease, lymphopenia and multisystemic organ involvement. The timely identification of such patients with an immunocytometric panel might be critical for targeted therapeutic management.


Subject(s)
Autoimmune Diseases , COVID-19 , Immunologic Deficiency Syndromes , Child , Humans , Interleukin-10 , SARS-CoV-2 , Interleukin-17 , Interleukin-6 , RNA, Viral , Cytokines/metabolism , Biomarkers , Autoantigens , Guanine Nucleotide Exchange Factors
13.
Front Immunol ; 13: 928171, 2022.
Article in English | MEDLINE | ID: covidwho-2080132

ABSTRACT

The fatal outcomes of COVID-19 are related to the high reactivity of the innate wing of immunity. Estrogens could exert anti-inflammatory effects during SARS-CoV-2 infection at different stages: from increasing the antiviral resistance of individual cells to counteracting the pro-inflammatory cytokine production. A complex relationship between sex hormones and immune system implies that menopausal hormone therapy (MHT) has pleiotropic effects on immunity in peri- and postmenopausal patients. The definite immunological benefits of perimenopausal MHT confirm the important role of estrogens in regulation of immune functionalities. In this review, we attempt to explore how sex hormones and MHT affect immunological parameters of the organism at different level (in vitro, in vivo) and what mechanisms are involved in their protective response to the new coronavirus infection. The correlation of sex steroid levels with severity and lethality of the disease indicates the potential of using hormone therapy to modulate the immune response and increase the resilience to adverse outcomes. The overall success of MHT is based on decades of experience in clinical trials. According to the current standards, MHT should not be discontinued in COVID-19 with the exception of critical cases.


Subject(s)
COVID-19 , COVID-19/drug therapy , Estrogens/therapeutic use , Gonadal Steroid Hormones , Humans , Immune System , Menopause , Pandemics , SARS-CoV-2
14.
Front Immunol ; 13: 861251, 2022.
Article in English | MEDLINE | ID: covidwho-2080128

ABSTRACT

COVID-19 is characterised by a broad spectrum of clinical and pathological features. Natural killer (NK) cells play an important role in innate immune responses to viral infections. Here, we analysed the phenotype and activity of NK cells in the blood of COVID-19 patients using flow cytometry, single-cell RNA-sequencing (scRNA-seq), and a cytotoxic killing assay. In the plasma of patients, we quantified the main cytokines and chemokines. Our cohort comprises COVID-19 patients hospitalised in a low-care ward unit (WARD), patients with severe COVID-19 disease symptoms hospitalised in intensive care units (ICU), and post-COVID-19 patients, who were discharged from hospital six weeks earlier. NK cells from hospitalised COVID-19 patients displayed an activated phenotype with substantial differences between WARD and ICU patients and the timing when samples were taken post-onset of symptoms. While NK cells from COVID-19 patients at an early stage of infection showed increased expression of the cytotoxic molecules perforin and granzyme A and B, NK cells from patients at later stages of COVID-19 presented enhanced levels of IFN-γ and TNF-α which were measured ex vivo in the absence of usual in vitro stimulation. These activated NK cells were phenotyped as CD49a+CD69a+CD107a+ cells, and their emergence in patients correlated to the number of neutrophils, and plasma IL-15, a key cytokine in NK cell activation. Despite lower amounts of cytotoxic molecules in NK cells of patients with severe symptoms, majority of COVID-19 patients displayed a normal cytotoxic killing of Raji tumour target cells. In vitro stimulation of patients blood cells by IL-12+IL-18 revealed a defective IFN-γ production in NK cells of ICU patients only, indicative of an exhausted phenotype. ScRNA-seq revealed, predominantly in patients with severe COVID-19 disease symptoms, the emergence of an NK cell subset with a platelet gene signature that we identified by flow and imaging cytometry as aggregates of NK cells with CD42a+CD62P+ activated platelets. Post-COVID-19 patients show slow recovery of NK cell frequencies and phenotype. Our study points to substantial changes in NK cell phenotype during COVID-19 disease and forms a basis to explore the contribution of platelet-NK cell aggregates to antiviral immunity against SARS-CoV-2 and disease pathology.


Subject(s)
COVID-19 , Humans , Granzymes/metabolism , Perforin/metabolism , Interleukin-15/metabolism , Interleukin-18/metabolism , SARS-CoV-2 , Tumor Necrosis Factor-alpha/metabolism , Blood Platelets/metabolism , Integrin alpha1/metabolism , Killer Cells, Natural , Cytokines/metabolism , Chemokines/metabolism , Interleukin-12/metabolism , Antiviral Agents/metabolism , RNA/metabolism
15.
J Infect Dis ; 2022 Oct 19.
Article in English | MEDLINE | ID: covidwho-2077789

ABSTRACT

BACKGROUND: Based on the fact that COVID-19 is still spreading despite vaccine worldwide administration, there is an imperative need to understand the underlying mechanisms of vaccine-induced inter-individual immune response variations. METHODS: We compared humoral and cellular immune responses in 127 individuals vaccinated with either BNT162b2, mRNA-1273 or ChAdOx1-nCoV-19 vaccine. RESULTS: We found that both mRNA vaccines induced faster and stronger humoral responses as assessed by high Spike- and RBD-specific antibody titers and neutralizing efficacy in comparison to ChAdOx1-nCoV-19 vaccine. At 7 months post vaccination, a decreasing trend in humoral responses was observed, irrespective of the vaccine administered. Correlation analysis between anti-S1 IgG and IFNγ production unveiled a heterogeneous immune profile among BNT162b2-vaccinated individuals. Specifically, vaccination in the high-responder group induced sizable populations of polyfunctional memory CD4+ TH1 cells, follicular helper T cells (TFH) and T cells with features of stemness along with high neutralizing antibody production that persisted up to 7 months.. In contrast, low responders were characterized by loss or significantly reduced antibody titers and memory T cells and a considerably lower capacity for IL-2 and IFNγ production. CONCLUSIONS: We identified that long-term humoral responses correlate with the individual's ability to produce antigen-specific persistent memory T cell populations.

16.
Endocrine ; 2022 Oct 18.
Article in English | MEDLINE | ID: covidwho-2075622

ABSTRACT

An outbreak of pneumonia caused by a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is called COVID-19 and has led to a pandemic worldwide. It is reasonable to investigate and control factors affecting disease severity and mortality. The relation between vitamin D and viral pneumonia has been previously reported. Vitamin D deficiency is common and may increase hospital admission and mortality rate in patients with COVID-19. This mini-review examines the pathways that show the association between vitamin D and COVID-19. On the other hand, it deals with the available evidence related to the relationship between vitamin D deficiency and the effect of vitamin D supplementation on the prevalence, severity, and mortality of COVID-19. Also, we described the pathophysiology of the organs' involvement in COVID-19 and the effect of vitamin D on these outcomes. Vitamin D strengthens the innate and adaptive immune system, modulates immune responses, prevents lung and cardiovascular system damage, and reduces thrombotic events. Vitamin D exerts these effects in several pathways. Vitamin D prevents virus entry and replication by maintaining the integrity of the body's physical barrier. Vitamin D reduces the damage to vital organs and thrombotic events by increasing the level of Angiotensin-converting enzyme 2 (ACE2), nitric oxide, and antioxidants or by reducing inflammatory cytokines and free radicals. Sufficient vitamin D may be reduced morbidity and mortality due to COVID-19. However, this issue should be investigated and confirmed by further research in the future.

17.
Excli Journal ; 21:1245-1272, 2022.
Article in English | Web of Science | ID: covidwho-2072283

ABSTRACT

The severe acute respiratory syndrome (SARS-CoV, now SARS-CoV-1), middle east respiratory syndrome (MERS-CoV), Neo-CoV, and 2019 novel coronavirus (SARS-CoV-2/COVID-19) are the most notable corona-viruses, infecting the number of people worldwide by targeting the respiratory system. All these viruses are of zoonotic origin, predominantly from bats which are one of the natural reservoir hosts for coronaviruses. Thus, the major goal of our review article is to compare and contrast the characteristics and attributes of these coronaviruses. The SARS-CoV-1, MERS-CoV, and COVID-19 have many viral similarities due to their classification, they are not genetically related. COVID-19 shares approximately 79 % of its genome with SARS-CoV-1 and about 50 % with MERS-CoV. The shared receptor protein, ACE2 exhibit the most striking genetic similarities between SARS-CoV-1 and SARS-CoV-2. SARS-CoV primarily replicates in the epithelial cells of the respiratory system, but it may also affect macrophages, monocytes, activated T cells, and dendritic cells. MERS-CoV not only infects and replicates inside the epithelial and immune cells, but it may lyse them too, which is one of the common reasons for MERS's higher mortality rate. The details of infections caused by SARS-CoV-2 and lytic replication mecha-nisms in host cells are currently mysterious. In this review article, we will discuss the comparative highlights of SARS-CoV-1, MERS-CoV, SARS-CoV-2, and Neo-CoV, concerning their structural features, morphological characteristics, sources of virus origin and their evolutionary transitions, infection mechanism, computational study approaches, pathogenesis and their severity towards several diseases, possible therapeutic approaches, and preventive measures.

18.
Bali Medical Journal ; 11(3):1059-1062, 2022.
Article in English | Web of Science | ID: covidwho-2072274

ABSTRACT

Background: Pregnant women infected with SARS-CoV-2 experienced increased pro-inflammatory cytokines, including TNF-alpha, resulting in a cytokine storm condition. This study aimed to compare TNF-alpha levels between pregnant women infected and not infected with COVID-19 in the third trimester.Method: This observational research was conducted with cross sectional design. Our study included pregnant women who came to the delivery room/inpatient at Dr. Soetomo General Hospital Surabaya before or during labor between May and June 2021. The inclusion criteria were third trimester gestational age or >28 weeks with SARS-RT-PCR nasopharyngeal swab result. The exclusion criteria were all significant pregnancy complications. The pregnant woman coming to the delivery room will be screened for COVID-19, and blood samples will be examined using the flow cytometry method for the cytokine Th1: TNF-alpha.Result: There were no significant differences in TNF-alpha levels in pregnant women who were infected and not infected with COVID-19 (median 3.42 (7.24) pg/ml vs. 2.70 (3.06) pg/ml. p=0.138). There was also no significant difference in TNF-alpha levels in pregnant women with symptomatic vs. asymptomatic COVID-19 infection (3.21(3.97) vs. 2.41(2.71) pg/ml;p=0.314).Conclusion: This study revealed no significant difference in TNF-alpha serum level between SARS-CoV-2 infected pregnant women with normal pregnant women.

19.
Pathophysiology ; 29(4): 583-594, 2022 Oct 11.
Article in English | MEDLINE | ID: covidwho-2071678

ABSTRACT

Cytokines are expressed by various cells after several stimuli such as surgical tissue damage, producing a systemic inflammatory response (SIR). C-reactive protein (CRP) is used extensively in clinical practice after operative injury, but proinflammatory cytokines, iron status, albumin, neutrophil-to-lymphocyte (N/L) ratio and hemoglobin, as acute phase reactants, have been poorly documented. This study aims to show how they behave after surgery, comparing laparoscopic (LC) versus open cholecystectomy (OC). In total, 55 patients were included in a prospective non-randomized form to undergo a cholecystectomy: 8 patients OC (50% females) and 47 patients LC (68% females). Before (A1) and 24 h after surgery (A2), blood samples were taken for an ordinary analysis and IL6, IL8 and TNFα determination. There were no differences between LC and OC groups concerning age, CRP, IL6 and TNFα at day A1. In the LC group at day A2, CRP, IL6, IL8, TNF, ferritin, leukocytes and N/L ratio increased; hemoglobin, lymphocytes, prothrombin and albumin decreased (p < 0.05). In the OC group at day A2, only IL6 (p < 0,07), ferritin, leukocytes, N/L ratio and CRP (p < 0.05) increased; serum iron, hemoglobin, lymphocytes and albumin (p < 0.05) decreased. At day A2, OC vs. LC group, higher values were observed in IL6, ferritin and CRP (p ≤ 0.05), and lesser values were observed in serum iron and prothrombin (p < 0.05). In conclusion, classic markers of inflammation are altered after surgery, in a milder way in laparoscopic surgery. Ferritin can be used as an inflammatory marker, as has been described in COVID-19 infection.

20.
J Clin Med ; 11(20)2022 Oct 14.
Article in English | MEDLINE | ID: covidwho-2071542

ABSTRACT

For 2.5 years we have been facing the coronavirus disease (COVID-19) and its health, social and economic effects. One of its known consequences is the development of neuropsychiatric diseases such as anxiety and depression. However, reports of manic episodes related to COVID-19 have emerged. Mania is an integral part of the debilitating illness-bipolar disorder (BD). Due to its devastating effects, it is therefore important to establish whether SARS-CoV-2 infection is a causative agent of this severe mental disorder. In this narrative review, we discuss the similarities between the disorders caused by SARS-CoV-2 and those found in patients with BD, and we also try to answer the question of whether SARS-CoV-2 infection may be a risk factor for the development of this affective disorder. Our observation shows that disorders in COVID-19 showing the greatest similarity to those in BD are cytokine disorders, tryptophan metabolism, sleep disorders and structural changes in the central nervous system (CNS). These changes, especially intensified in severe infections, may be a trigger for the development of BD in particularly vulnerable people, e.g., with family history, or cause an acute episode in patients with a pre-existing BD.

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