scholarly journals Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications

2021 ◽  
Vol 22 (21) ◽  
pp. 12081
Author(s):  
Yasutomi Higashikuni ◽  
Wenhao Liu ◽  
Takumi Obana ◽  
Masataka Sata
Keyword(s):  
Endothelial Dysfunction ◽  
Immune Responses ◽  
Current Knowledge ◽  
Multiple Organ ◽  
Endothelial Injury ◽  
Economic Activities ◽  
High Grade Fever ◽  
Mortality And Morbidity ◽  
Therapeutic Implications ◽  
Global Pandemic

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough, and spontaneously resolve within ten days. However, in severe cases, COVID-19 leads to atypical bilateral interstitial pneumonia, acute respiratory distress syndrome, and systemic thromboembolism, resulting in multiple organ failure with high mortality and morbidity. SARS-CoV-2 has immune evasion mechanisms, including inhibition of interferon signaling and suppression of T cell and B cell responses. SARS-CoV-2 infection directly and indirectly causes dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction, which interact with each other and are exacerbated by cardiovascular risk factors. In this review, we summarize current knowledge on the pathogenic basis of thromboinflammation and endothelial injury in COVID-19. We highlight the distinct contributions of dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction to the pathogenesis of COVID-19. In addition, we discuss potential therapeutic strategies targeting these mechanisms.

scholarly journals An A-E assessment of post-ICU COVID-19 recovery

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Matthew Cadd ◽  
Maya Nunn
Keyword(s):  
Critical Care ◽  
Current Knowledge ◽  
Multiple Organ ◽  
Long Term Effects ◽  
Care Services ◽  
Global Pandemic ◽  
Wide Range ◽  
Assessment And Treatment ◽  
Critical Care Admission

AbstractThe COVID-19 global pandemic has placed unprecedented strain on healthcare and critical care services around the world. Whilst most resources have focused on the acute phase of the disease, there is likely to be an untold burden of patients chronically affected.A wide range of sequelae contribute to post intensive care syndrome (PICS); from our current knowledge of COVID-19, a few of these have the potential to be more prevalent following critical care admission. Follow-up assessment, diagnosis and treatment in an increasingly virtual setting will provide challenges but also opportunities to develop these services. Here, we propose an A to E approach to consider the potential long-term effects of COVID-19 following critical care admission.Anxiety and other mental health diagnosesBreathlessnessCentral nervous system impairmentDietary insufficiency and malnutritionEmbolic eventsDeveloping strategies to mitigate these during admission and providing follow-up, assessment and treatment of persistent multiple organ dysfunction will be essential to improve morbidity, mortality and patient quality of life.

scholarly journals Understanding Host Immunity and the Gut Microbiota Inspires the New Development of Vaccines and Adjuvants

Pharmaceutics ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 163
Author(s):  
Kyosuke Yakabe ◽  
Jun Uchiyama ◽  
Masahiro Akiyama ◽  
Yun-Gi Kim
Keyword(s):  
Gut Microbiota ◽  
Immune Responses ◽  
Immune Cells ◽  
Current Knowledge ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Mortality And Morbidity ◽  
Complex Interactions ◽  
Immunological Mechanisms ◽  
New Development

Vaccinations improve the mortality and morbidity rates associated with several infections through the generation of antigen-specific immune responses. Adjuvants are often used together with vaccines to improve immunogenicity. However, the immune responses induced by most on-going vaccines and adjuvants approved for human use vary in individuals; this is a limitation that must be overcome to improve vaccine efficacy. Several reports have indicated that the symbiotic bacteria, particularly the gut microbiota, impact vaccine-mediated antigen-specific immune responses and promote the induction of nonspecific responses via the “training” of innate immune cells. Therefore, the interaction between gut microbiota and innate immune cells should be considered to ensure the optimal immunogenicity of vaccines and adjuvants. In this review, we first introduce the current knowledge on the immunological mechanisms of vaccines and adjuvants. Subsequently, we discuss how the gut microbiota influences immunity and highlight the relationship between gut microbes and trained innate immunity, vaccines, and adjuvants. Understanding these complex interactions will provide insights into novel vaccine approaches centered on the gut microbiota.

scholarly journals Histone deacetylases in modulating cardiac disease and their clinical translational and therapeutic implications

2020 ◽  
pp. 153537022094412
Author(s):  
Zhengke Wang ◽  
Yu Tina Zhao ◽  
Ting C Zhao
Keyword(s):  
Cardiac Disease ◽  
Histone Deacetylases ◽  
Cardiac Development ◽  
Current Knowledge ◽  
Hdac Inhibitors ◽  
Current View ◽  
Cardiovascular Development ◽  
Mortality And Morbidity ◽  
Therapeutic Implications ◽  
Response To Stress

Cardiovascular diseases are the leading cause of mortality and morbidity worldwide. Histone deacetylases (HDACs) play an important role in the epigenetic regulation of genetic transcription in response to stress or pathological conditions. HDACs interact with a complex co-regulatory network of transcriptional regulators, deacetylate histones or non-histone proteins, and modulate gene expression in the heart. The selective HDAC inhibitors have been considered to be a critical target for the treatment of cardiac disease, especially for ameliorating cardiac dysfunction. In this review, we discuss our current knowledge of the cellular and molecular basis of HDACs in mediating cardiac development and hypertrophy and related pharmacologic interventions in heart disease. Impact statement Histone deacetylases (HDACs) have recently been recognized as one of the most important regulated mechanism(s) in mediating cardiovascular development, myocardial injury, and hypertrophy. This detailed review of the functional role(s) and molecular mechanism(s) of histone deacetylase will provide the current view by which HDACs induce different biological signaling in the regulation of cardiac physiology and disease. More importantly, HDACs could be targeted to develop a new therapeutic strategy in treating cardiovascular disorders. Further studies of the specific roles and targets of HDACs will extend our knowledge of the biological impact and clinical implications of HDACs.

scholarly journals Cardiac Cell Therapy: Insights into the Mechanisms of Tissue Repair

2021 ◽  
Vol 22 (3) ◽  
pp. 1201
Author(s):  
Hsuan Peng ◽  
Kazuhiro Shindo ◽  
Renée R. Donahue ◽  
Ahmed Abdel-Latif
Keyword(s):  
Stem Cell ◽  
Immune Responses ◽  
Tissue Repair ◽  
Molecular Mechanisms ◽  
Clinical Evidence ◽  
Current Knowledge ◽  
Cell Delivery ◽  
Cardiac Cell Therapy ◽  
Stem Cell Treatment

Stem cell-based cardiac therapies have been extensively studied in recent years. However, the efficacy of cell delivery, engraftment, and differentiation post-transplant remain continuous challenges and represent opportunities to further refine our current strategies. Despite limited long-term cardiac retention, stem cell treatment leads to sustained cardiac benefit following myocardial infarction (MI). This review summarizes the current knowledge on stem cell based cardiac immunomodulation by highlighting the cellular and molecular mechanisms of different immune responses to mesenchymal stem cells (MSCs) and their secretory factors. This review also addresses the clinical evidence in the field.

scholarly journals Potential Role and Impact of Peripheral Blood Mononuclear Cells in Radiographic Axial Spondyloarthritis-Associated Endothelial Dysfunction

Diagnostics ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1037
Author(s):  
Patricia Ruiz-Limon ◽  
Maria L. Ladehesa-Pineda ◽  
Clementina Lopez-Medina ◽  
Chary Lopez-Pedrera ◽  
Maria C. Abalos-Aguilera ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Axial Spondyloarthritis ◽  
Endothelial Injury ◽  
In Vitro Studies ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Endothelial dysfunction (ED) is well known as a process that can lead to atherosclerosis and is frequently presented in radiographic axial spondyloarthritis (r-axSpA) patients. Here, we investigated cellular and molecular mechanisms underlying r-axSpA-related ED, and analyzed the potential effect of peripheral blood mononuclear cells (PBMCs) in promoting endothelial injury in r-axSpA. A total of 30 r-axSpA patients and 32 healthy donors (HDs) were evaluated. The endothelial function, inflammatory and atherogenic profile, and oxidative stress were quantified. In vitro studies were designed to evaluate the effect of PBMCs from r-axSpA patients on aberrant endothelial activation. Compared to HDs, our study found that, associated with ED and the plasma proatherogenic profile present in r-axSpA, PBMCs from these patients displayed a pro-oxidative, proinflammatory, and proatherogenic phenotype, with most molecular changes noticed in lymphocytes. Correlation studies revealed the relationship between this phenotype and the microvascular function. Additional in vitro studies confirmed that PBMCs from r-axSpA patients promoted endothelial injury. Altogether, this study suggests the relevance of r-axSpA itself as a strong and independent cardiovascular risk factor, contributing to a dysfunctional endothelium and atherogenic status by aberrant activation of PBMCs. Lymphocytes could be the main contributors in the development of ED and subsequent atherosclerosis in this pathology.

scholarly journals Influenza vaccination and the risk of COVID-19 infection and severe illness in older adults in the United States

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kelly Huang ◽  
Shu-Wen Lin ◽  
Wang-Huei Sheng ◽  
Chi-Chuan Wang
Keyword(s):  
Immune Responses ◽  
Influenza Vaccine ◽  
Influenza Vaccination ◽  
The United States ◽  
Cross Sectional Study ◽  
Severe Illness ◽  
Cross Sectional ◽  
Global Pandemic ◽  
Study Population ◽  
Health Database

AbstractThe coronavirus disease of 2019 (COVID-19) has caused a global pandemic and led to nearly three million deaths globally. As of April 2021, there are still many countries that do not have COVID-19 vaccines. Before the COVID-19 vaccines were developed, some evidence suggested that an influenza vaccine may stimulate nonspecific immune responses that reduce the risk of COVID-19 infection or the severity of COVID-19 illness after infection. This study evaluated the association between influenza vaccination and the risk of COVID-19 infection. We conducted a retrospective cross-sectional study with data from July 1, 2019, to June 30, 2020 with the Claims data from Symphony Health database. The study population was adults age 65 years old or older who received influenza vaccination between September 1 and December 31 of 2019. The main outcomes and measures were odds of COVID-19 infection and severe COVID-19 illness after January 15, 2020. We found the adjusted odds ratio (aOR) of COVID-19 infection risk between the influenza-vaccination group and no-influenza-vaccination group was 0.76 (95% confidence interval (CI), 0.75–0.77). Among COVID-19 patients, the aOR of developing severe COVID-19 illness was 0.72 (95% CI, 0.68–0.76) between the influenza-vaccination group and the no-influenza-vaccination group. When the influenza-vaccination group and the other-vaccination group were compared, the aOR of COVID-19 infection was 0.95 (95% CI, 0.93–0.97), and the aOR of developing a severe COVID-19 illness was 0.95 (95% CI, 0.80–1.13). The influenza vaccine may marginally protect people from COVID-19 infection.

scholarly journals Arginase 1 (Arg1) as an Up-Regulated Gene in COVID-19 Patients: A Promising Marker in COVID-19 Immunopathy

2021 ◽  
Vol 10 (5) ◽  
pp. 1051 ◽  
Author(s):  
Afshin Derakhshani ◽  
Nima Hemmat ◽  
Zahra Asadzadeh ◽  
Moslem Ghaseminia ◽  
Mahdi Abdoli Shadbad ◽  
...  
Keyword(s):  
Immune Responses ◽  
Whole Blood ◽  
Roc Analysis ◽  
Operating Characteristic ◽  
Rna Extraction ◽  
Diagnostic Value ◽  
Healthy Individuals ◽  
Cdna Synthesis ◽  
Arginase 1 ◽  
Global Pandemic

Background: The coronavirus disease 2019 (COVID-19) outbreak, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been declared a global pandemic. It is well-established that SARS-CoV-2 infection can lead to dysregulated immune responses. Arginase-1 (Arg1), which has a pivotal role in immune cells, can be expressed in most of the myeloid cells, e.g., neutrophils and macrophages. Arg1 has been associated with the suppression of antiviral immune responses. Methods: Whole blood was taken from 21 COVID-19 patients and 21 healthy individuals, and after RNA extraction and complementary DNA (cDNA) synthesis, gene expression of Arg1 was measured by real-time PCR. Results: The qPCR results showed that the expression of Arg1 was significantly increased in COVID-19 patients compared to healthy individuals (p < 0.01). The relative expression analysis demonstrated there were approximately 2.3 times increased Arg1 expression in the whole blood of COVID-19 patients. Furthermore, the receiver operating characteristic (ROC) analysis showed a considerable diagnostic value for Arg1 expression in COVID-19 (p = 0.0002 and AUC = 0.8401). Conclusion: Arg1 might be a promising marker in the pathogenesis of the disease, and it could be a valuable diagnostic tool.

COVID-19 and nutritional deficiency: a review of existing knowledge

2021 ◽  
Vol 42 (1) ◽  
pp. 77-85
Author(s):  
Meghana Muthuvattur Pallath ◽  
Ashok Kumar Ahirwar ◽  
Satyendra Chandra Tripathi ◽  
Priyanka Asia ◽  
Apurva Sakarde ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Infection ◽  
Close Contact ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Antibody Affinity ◽  
Global Pandemic ◽  
Underlying Diseases ◽  
Pro Inflammatory Cytokines

Abstract COVID-19 has resulted in an ongoing global pandemic, which spread largely among people who have had close contact with the infected person. The immunopathology of the SARS-CoV-2 virus includes the production of an excess amount of pro-inflammatory cytokines “a cytokine-storm”. The respiratory system (main), cardiovascular system and the gastrointestinal tract are the most affected body systems during viral infection. It has been found that most of the patients who require admission to hospital are elderly or have chronic underlying diseases. Higher cases of malnutrition and co-morbidities like diabetes mellitus and cardiovascular diseases are reported in elderly patients due to which, the immune system weakens and hence, the response to the virus is diminished in magnitude. A deficiency of micronutrients results in impaired immune responses leading to improper secretion of cytokines, alterations in secretory antibody response and antibody affinity which increases susceptibility to viral infection. The deficiency of various micronutrients in COVID-19 patient can be treated by appropriate nutritional supplements, prescribed after evaluating the patients’ nutritional status. Here we aim to highlight the role of a few particular nutrients namely Vitamin D, Vitamin C, Omega-3 fatty acids, Zinc and Magnesium along with the synergistic roles they play in enhancing immunity and thus, maintaining homeostasis.

scholarly journals Suicidal Erythrocyte Death in Metabolic Syndrome

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 154
Author(s):  
Ignazio Restivo ◽  
Alessandro Attanzio ◽  
Luisa Tesoriere ◽  
Mario Allegra
Keyword(s):  
Metabolic Syndrome ◽  
Cell Death ◽  
Endothelial Dysfunction ◽  
Cell Membrane ◽  
Clinical Evidence ◽  
Current Knowledge ◽  
Vascular Complications ◽  
Cardiovascular Complications ◽  
Inflammatory Milieu ◽  
Cardiometabolic Factors

Eryptosis is a coordinated, programmed cell death culminating with the disposal of cells without disruption of the cell membrane and the release of endocellular oxidative and pro-inflammatory milieu. While providing a convenient form of death for erythrocytes, dysregulated eryptosis may result in a series of detrimental and harmful pathological consequences highly related to the endothelial dysfunction (ED). Metabolic syndrome (MetS) is described as a cluster of cardiometabolic factors (hyperglycemia, dyslipidemia, hypertension and obesity) that increases the risk of cardiovascular complications such as those related to diabetes and atherosclerosis. In the light of the crucial role exerted by the eryptotic process in the ED, the focus of the present review is to report and discuss the involvement of eryptosis within MetS, where vascular complications are utterly relevant. Current knowledge on the mechanisms leading to eryptosis in MetS-related conditions (hyperglycemia, dyslipidemia, hypertension and obesity) will be analyzed. Moreover, clinical evidence supporting or proposing a role for eryptosis in the ED, associated to MetS cardiovascular complications, will be discussed.

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