Serum inflammatory factors are positively correlated with the production of specific antibodies in coronavirus disease 2019 patients.
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ABSTRACT:
SUBMITTER: Zheng M
PROVIDER: S-EPMC7506822 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description: Not available
| S-EPMC7245297 | biostudies-literature
Project description:The pandemic of COVID-19 caused by SARS-CoV-2 has made serious threats to the public health. Antibodies have been considered as promising therapeutics for the prevention and treatment of pathogens. So far, effectors that can influence the sustainability of SARS-CoV-2 specific antibodies in COVID-19 patients are still unclear. In this paper, we attempted to find potential key factors correlated with SARS-CoV-2 specific antibodies. Transcriptional analysis with the peripheral blood mononuclear cells (PBMCs) revealed proportional changes of immune cell subsets in COVID-19 convalescent patients, including a substantial decrease of monocytes and evident increase of dendritic cells (DCs). Moreover, we found that the gene expressions of chemokines associated with monocyte/macrophage were significantly up-regulated during the COVID-19 recovery phase. Most importantly, we found a set of 27 immune genes corresponding to a comparatively lower amount of SARS-CoV-2 specific antibodies, and identified two hub genes, IL1β and IL6, the protein expressions of which exhibited negative correlation with the immunoglobulin G (IgG) levels in COVID-19 convalescent sera. In addition, we found that high expressions of these 2 hub genes during the convalescent stage were negatively associated with the plasma cell marker CD138. Our study presented two key inflammatory factors correlated to the low level of SARS-CoV-2 specific antibodies, which indicated the potential regulatory process of plasmatic antibodies levels in some COVID-19 convalescent patients.
| S-EPMC7832135 | biostudies-literature
Project description:Use of interleukin (IL-6) inhibitors has become one of the most complicated clinical issues in treating coronavirus disease 2019 (COVID-19). Recently, randomized open-label platform trials have found that IL-6 inhibitors have a beneficial effect on mortality in severe COVID-19. However, several questions arise around their mechanism of action in this disease, as well as how, when, and at which dose they should be used. IL-6 has both proinflammatory and anti-inflammatory effects, which may modulate the course of COVID-19, whose immunopathogenesis is driven by the innate immune system, autoantibodies, and interferon. Given that patients with delayed seroconversion against the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein would be at the highest risk of complications beyond the second week of disease, we propose that considering patient serostatus at admission could optimize the use of IL-6 inhibitors in COVID-19. We predict that the net treatment benefits could be higher in the subgroup of patients with delayed seroconversion as compared to those who seroconvert more rapidly after SARS-CoV-2 infection.
| S-EPMC8992338 | biostudies-literature
Project description:A molecular mimicry between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and human proteins supports the possibility that autoimmunity takes place during coronavirus disease 2019 (COVID-19) contributing to tissue damage. For example, anti-phospholipid antibodies (aPL) have been reported in COVID-19 as a result of such mimicry and thought to contribute to the immunothrombosis characteristic of the disease. Consistently, active immunization with the virus spike protein may elicit the production of cross-reactive autoantibodies, including aPL. We prospectively looked at the aPL production in healthcare workers vaccinated with RNA- (BNT162b2, n. 100) or adenovirus-based vaccines (ChAdOx1, n. 50). Anti-cardiolipin, anti-beta2 glycoprotein I, anti-phosphatidylserine/prothrombin immunoglobulin G (IgG), IgA, and IgM before and after vaccination were investigated. Anti-platelet factor 4 immunoglobulins were also investigated as autoantibodies associated with COVID-19 vaccination. Additional organ (anti-thyroid) and non-organ (anti-nuclear) autoantibodies and IgG against human proteome were tested as further post-vaccination autoimmunity markers. The antibodies were tested one or three months after the first injection of ChAdOx1 and BNT162b2, respectively; a 12-month clinical follow-up was also performed. Vaccination occasionally induced low titers of aPL and other autoantibodies but did not affect the titer of pre-existing autoantibodies. No significant reactivities against a microarray of approximately 20,000 human proteins were found in a subgroup of ChAdOx1-vaccinees. Consistently, we did not record any clinical manifestation theoretically associated with an underlying autoimmune disorder. The data obtained after the vaccination (two doses for the RNA-based and one dose for the adenovirus-based vaccines), and the clinical follow-up are not supporting the occurrence of an early autoimmune response in this cohort of healthcare workers.
| S-EPMC9334668 | biostudies-literature
Project description:AbstractThis study aims to compare the receptor-binding domain (RBD) severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-specific antibody titers in human milk between mothers with a confirmed coronavirus disease 2019 (COVID-19) polymerase chain reaction (PCR) test and mothers with viral symptoms suggestive of COVID-19. The area under the curve (AUC) for RBD SARS-CoV-2-specific secretory immunoglobulin A (SIgA)/immunoglobulin A (IgA), secretory immunoglobulin M (SIgM)/immunoglobulin M (IgM), immunoglobulin G (IgG), and free secretory components (fSC) in milk samples from eight mothers with a confirmed COVID-19 PCR, eight mothers with viral symptoms (no PCR testing), and six unexposed mothers (pre-pandemic 2018). AUCs of RBD SARS-CoV-2-specific SIgA/IgA, SIgM/IgM, IgG, and fSC in milk samples were comparable between mothers with confirmed COVID-19 PCR and mothers with viral symptoms of suggestive COVID-19. AUCs of RBD-specific SIgA/IgA, IgG, and fSC were higher in the COVID-19-exposed group than in the unexposed group, and SIgM/IgM tended to be higher in the exposed mothers. In conclusion, women with viral symptoms suggestive of COVID-19 could secrete antibodies and fSC specific to SARS-CoV-2 in human milk.
| S-EPMC8195680 | biostudies-literature
Project description:BackgroundPhysiologically, the levels of homocysteine (Hcy) and serum uric acid (SUA) are closely related; however, clinical studies on the relationship between Hcy and SUA have drawn different conclusions and have not analyzed this association among adolescents. This study therefore aimed to evaluate the relationship between Hcy and SUA levels among adolescents.MethodsIn this study, we performed a cross-sectional analysis of data from the National Health and Nutrition Examination Survey for the period 1999-2006, which included 5,404 adolescents aged 12-19 years. An elevated SUA level was defined as ≥5.5 mg/dL. Multivariate logistic regression and multivariate linear regression models were also applied in this study.ResultsThe mean concentrations of Hcy and SUA were 6.0 μmol/L and 5.0 mg/dL, respectively, and 33.6% of the participants had SUA levels of ≥5.5 mg/dL. There was a dose-response relationship between Hcy and SUA, and Hcy was linearly positively correlated with SUA. The β value [95% confidence interval (CI)] for SUA in the fully adjusted model was1.43 (95% CI: 1.18, 1.68). The multivariate logistic regression model showed that per 1 increment in log-transformed Hcy, the risk of elevated SUA levels increased by 8.80 times (odds ratio, 8.80, 95% CI: 4.25, 18.20). Subgroup analyses showed that the relationship between Hcy and SUA was significantly different according to sex, age, body mass index (BMI), and estimated glomerular filtration rate (eGFR) stratification (P for interaction <0.05).ConclusionHcy levels were positively correlated with SUA levels and elevated SUA levels among U.S. teenagers, and this effect was more significant among boys aged ≥17 years and among people with lower BMI and eGFR.
| S-EPMC9001925 | biostudies-literature
Project description:BackgroundSilent Information Regulator 2 (SIRT2) protein inhibition has been shown to play a neuroprotective role in acute ischemic stroke (AIS) in mice. However, its role in AIS patients has not been fully understood. In this study, we aimed to analyze SIRT2 protein expression in serum exosomes of AIS and non-AIS patients, and evaluate its potential role in diagnosis and prognosis of AIS.MethodsSerum exosomes from 75 non-AIS subjects and 75 AIS patients were isolated. The SIRT2 protein levels in exosomes were analyzed using enzyme linked immunosorbent assay (ELISA). The National Institutes of Health Stroke Scale (NIHSS) was used to evaluate the severity of the disease. The modified Rankin Scale (mRS) was employed to assess the functional outcomes of the patients at 3-months following stroke onset.ResultsThe SIRT2 protein concentration of serum exosomes were higher in AIS patients than non-AIS patients (p < 0.001). Furthermore, the receiver operative characteristic curve (ROC) demonstrated that higher serum exosome SIRT2 could differentiate AIS patients from non-AIS patients with a sensitivity of 81.3% and a specificity of 75.3%. The area under the curve was 0.838 (95% CI: 0.775, 0.902). Additionally, higher SIRT2 concentration of serum exosomes were associated with NIHSS ≥ 4 (p < 0.001) and mRS ≥ 3 (p = 0.025) in AIS patients. The ROC analysis showed SIRT2 could discriminate stroke with NIHSS ≥ 4 from mild stroke (NIHSS < 4) with a sensitivity of 75.0% and a specificity of 69.6%. The area under the curve was 0.771 (95% CI: 0.661,0.881). Similarly, the test showed SIRT2 could differentiate between AIS patients with mRS ≥ 3 from those with mRS < 3 with a sensitivity of 78.3% and a specificity of 51.9%. The area under the curve was 0.663 (95% CI: 0.531,0.796). The logistic regression analysis revealed that SIRT2 concentration in serum exosomes can independently predict the diagnosis of AIS (odd ratio = 1.394, 95%CI 1.231-1.577, p < 0.001) and higher NIHSS scores (≥ 4) (odd ratio = 1.258, 95%CI 1.084-1.460, p = 0.002). However, it could not independently predict the prognosis of AIS (odd ratio = 1.065, 95%CI 0.983-1.154, p = 0.125).ConclusionThe elevation of SIRT2 in serum exosomes may be a valuable biomarker of AIS, which may be a potential diagnostic tool to facilitate decision making for AIS patients.
| S-EPMC10485972 | biostudies-literature
Project description:BackgroundDuring the ongoing coronavirus disease 2019 (COVID-19) pandemic, many individuals were infected with and have cleared the virus, developing virus-specific antibodies and effector/memory T cells. An important unanswered question is what levels of T-cell and antibody responses are sufficient to protect from the infection.MethodsIn 5340 Moscow residents, we evaluated anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) immunoglobulin M (IgM)/immunoglobulin G (IgG) titers and frequencies of the T cells specific to the membrane, nucleocapsid, and spike proteins of SARS-CoV-2, using interferon gamma (IFN-γ) enzyme-linked immunosorbent spot (ELISpot) assay. Additionally, we evaluated the fractions of virus-specific CD4+ and CD8+ T cells using intracellular staining of IFN-γ and interleukin 2 followed by flow cytometry. We analyzed the COVID-19 rates as a function of the assessed antibody and T-cell responses, using the Kaplan-Meier estimator method, for up to 300 days postinclusion.ResultsWe showed that T-cell and antibody responses are closely interconnected and are commonly induced concurrently. Magnitudes of both responses inversely correlated with infection probability. Individuals positive for both responses demonstrated the highest levels of protectivity against the SARS-CoV-2 infection. A comparable level of protection was found in individuals with antibody response only, whereas the T-cell response by itself granted only intermediate protection.ConclusionsWe found that the contribution of the virus-specific antibodies to protection against SARS-CoV-2 infection is more pronounced than that of the T cells. The data on the virus-specific IgG titers may be instructive for making decisions in personalized healthcare and public anti-COVID-19 policies. Clinical Trials Registration. NCT04898140.
| S-EPMC9047235 | biostudies-literature
Project description:Objective: To study the potential effect of COVID-19 on the endometrium of affected symptomatic women. Design: Preliminary study of the endometrial transcriptomes in women with COVID-19 through RNA sequencing. Setting: Hospital and university laboratories. Subjects: Women with COVID-19 lacking SARS-CoV-2 infection in endometrial tissue. Intervention/Exposure: Endometrial biopsy collection. Main outcomes measures: Endometrial gene expression and functional analysis of patients with COVID-19 versus uninfected individuals. Results: COVID-19 systemic disease alters endometrial gene expression in 75% of women, with patients exhibiting a preponderance of 163 up-regulated (e.g., UTS2, IFI6, IFIH1, BNIP3) and 72 down-regulated genes (e.g., CPZ, CDH3, IRF4) (FDR<0.05). A total of 161 dysregulated functions (36 up-regulated and 125 down-regulated) were typically enriched in COVID-19 endometria, including upregulation in pathways involved in response to virus and cytokine inflammation, highlighting upregulation of a COVID-19 response pathway. Conclusion: COVID-19 affects endometrial gene expression despite the absence of SARS-CoV-2 particles in endometrial tissues.
2024-04-22 | GSE202553 | GEO
Project description:IntroductionReports of unexpected side effects have accompanied the vaccination of larger proportions of the population against coronavirus disease 2019 (COVID-19), including a few cases of inflammatory myopathy (IM). In a bid to improve understanding of the clinical course of vaccine complications, a systematic review of reported cases of IM following COVID-19 vaccination has been conducted.MethodsThe PRISMA guideline 2020 was followed. Two independent investigators systematically searched PubMed and Embase to identify relevant studies published up to July 2022, using the following keywords: COVID-19 Vaccine, inflammatory myositis. The Joanna Briggs Institute critical appraisal tools were used for the risk of bias.ResultsA total of 24 articles presenting clinical features of 37 patients with IM following COVID-19 vaccine were identified. Female patients composed 59.5% of cases and 82.4% had been vaccinated with BNT162b2 or ChAdOx1. Onset of symptoms occurred within 2 weeks of the first or second vaccine dose in 29 (85.3%) patients and included muscular weakness in 54.1% and skin rash in 71.4% of patients. Myositis specific autoantibodies (MSAs) and myositis associated autoantibodies (MAAs) were reported in 28 patients. Specific clinical subtypes of myositis, reported in 27 patients, included 22 (81.5%) cases of dermatomyositis (DM) and 3 (11.1%) cases of immune-mediated necrotizing myopathy (IMNM). Following treatment, 32 (86.5%) patients showed improvement on follow-up.ConclusionCOVID-19 vaccine may induce various clinical myositis subtypes and related antibodies. Muscular weakness was the most common presenting symptom. Clinicians should be aware of this unexpected adverse event following COVID-19 vaccination and arrange for appropriate management.Systematic review registrationINPLASY https://inplasy.com/inplasy-2022-9-0084/ [INPLASY202290084].
| S-EPMC9634642 | biostudies-literature