Question: What is the mechanism of inflammatory response and pathogenesis of COVID-19 cases?

A study suggests that overexpression of Kv1.3 channels in lymphocytes leads to overactivation of cellular immunity and cytokine storm in severe cases of COVID-19. Previous research shows that chloroquine and azithromycin suppress Kv1.3 channel activity and cytokine production from lymphocytes. This mechanism could explain the effectiveness of these drugs in treating severe COVID-19 cases.

A gene network approach was used to identify potential inflammatory mechanisms and bioactive genes in COVID-19 hyperinflammation. Network analysis of SARS-CoV-2 receptors led to the mining of a neutrophil-response signature and relevant inflammatory genes. RNA-seq data sets of lung cells infected with SARS-CoV-2 and bronchoalveolar lavage fluid cells from COVID-19 patients revealed up

The passage discusses a study on the dynamic immune response in three COVID-19 patients. SARS-CoV-2 infection triggers a highly dynamic early immune response. Virus persisted for 3-4 weeks in all patients, and cytokine expression was increased in the more severe case. Most inflammatory genes peaked after respiratory function declined, except for those in the IL1 pathway. CD4 and CD8 expression suggested a link between

The passage discusses a study on the dynamic immune response in three COVID-19 patients. SARS-CoV-2 infection was found to persist for 3-4 weeks, and the early response was highly dynamic with increased cytokine expression, especially in the most severe case. However, most inflammatory gene expression peaked after respiratory function declined, except for the IL1 pathway. The study suggests that IL1 and related pro-inflam

The passage discusses the limited data available on the impact of the immunomodulating drug dupilumab, which blocks IL-4 and IL-13, on the risk and progression of Coronavirus Disease 2019 (COVID-19). While the primary immune response to COVID-19 is Th1/Th17, IL-4 and IL-13, as Th2 cytokines, are not considered part of the

The passage discusses how patients with COVID-19 who sustain orthopaedic trauma injuries may experience an amplified inflammatory and hypercoagulable response due to their baseline hyperinflammatory state. This could make them more susceptible to thromboembolic disease and acute respiratory distress, and compromise their ability to withstand surgical intervention. The article reviews the current evidence on the pathogenesis of COVID-19 and its implications

The passage discusses how patients with COVID-19 who sustain orthopaedic trauma injuries may experience an amplified inflammatory and hypercoagulable response due to their baseline hyperinflammatory state. This could make them more susceptible to thromboembolic disease and acute respiratory distress, and compromise their ability to withstand surgical intervention. The passage also reviews the current evidence on the pathogenesis of COVID-19 and its

The passage discusses the potential for drug interactions in COVID-19 patients due to the impact of the disease on the cytochrome P450 metabolic machinery in the liver. The immune response to COVID-19, which can lead to a hyperinflammatory state, may cause significant derangements in the liver's ability to metabolize drugs, leading to unpredictable therapeutic or toxic responses. The authors suggest that COVID-19 patients may

COVID-19, caused by SARS-CoV-2, is a contagious respiratory disease where the immune system's role cannot be underestimated. Coronaviruses evade the immune system by inhibiting type I interferons, allowing uncontrolled viral replication. Severe cases result from massive viral replication leading to hyperinflammation or "cytokine storm." A weakened innate immune response is the primary cause

COVID-19 is linked to a hypercoagulable inflammatory state with microangiopathic pulmonary changes, which can lead to diffuse alveolar damage. The complement pathway, specifically the anaphylatoxins C3a and C5a, is implicated in COVID-19's pathogenesis. C5a triggers a cytokine storm and inflammatory response, but excessive C5a can lead

COVID-19 is linked to a hypercoagulable inflammatory state with microangiopathic pulmonary changes, which can lead to diffuse alveolar damage. The complement pathway, specifically the anaphylatoxins C3a and C5a, is implicated in COVID-19's pathogenesis. C5a triggers a cytokine storm and a hyper-inflammatory response, but excessive C5

The passage discusses the new complications arising from COVID-19, specifically the combination of systemic inflammatory response syndrome, disseminated intravascular coagulation (DIC), and thrombotic microangiopathy (TMA) in severe cases. TMA is a condition characterized by thrombocytopenia, hemolytic anemia, and organ failure. The article outlines the main types of TMA, their path

The passage summarizes a article about the cytokine storm, an excessive immune response leading to high mortality. During the COVID-19 epidemic, some severe cases have been linked to this condition. The article aims to explain the mechanisms behind COVID-19-induced inflammatory storm and propose treatment strategies.

The passage discusses the cytokine storm, an extreme immune response to external stimuli, and its connection to high mortality in COVID-19 patients. The article aims to provide insight into the mechanisms behind COVID-19-induced inflammatory storms and potential treatment strategies.

The passage discusses how positive-sense single-stranded RNA viruses, which include emerging human pathogens, evade the innate immune response, specifically the interferon response, to optimize their replication. The article reviews current knowledge on the role of interferons and host immune evasion in the pathogenesis of coronaviruses, alphaviruses, and flaviviruses. Despite the importance of understanding the effects of immune evasion on

A study was conducted to investigate the role of vitamin E acetate (VEA) and medium-chain triglycerides (MCT) in e-cigarette-related lung injury (EVALI). The findings suggest that these components induce pulmonary toxicity through oxidative damage and inflammatory responses, leading to acute lung injury. Exposure to e-cigarette cartridge aerosols generated reactive oxygen species,

This review article suggests that hemophagocytic lymphohistiocytosis (HLH), a severe inflammatory syndrome characterized by intense cytokine release, could be a complication in patients with severe COVID-19. The clinical characteristics of severe COVID-19 cases, such as fever, dyspnea, and multi-organ failure, resemble those of secondary HLH. The pathogenesis of SARS-CoV-2

MERS-CoV infection is linked to suppressed Th1 and Th2 cytokine/chemokine responses and heightened inflammatory innate immune reaction in the lower respiratory tract. Using RT2 Profiler PCR Arrays, this study provides initial insights into the pulmonary gene expression profile of Th1 and Th2 responses during acute MERS-CoV infection. Results indicate a downregulation of Th2, insufficient Th1 response,

The passage discusses COVID-19, caused by SARS-CoV-2, as a global pandemic with unknown damage mechanisms. It binds to angiotensin-converting enzyme 2 receptors, invades alveolar epithelial cells, and triggers a cytokine storm leading to severe lung injury, acute respiratory distress syndrome, septic shock, metabolic acidosis, coagulation dysfunction

A study using peripheral blood mononuclear cells (PBMCs) from COVID-19 patients identified 251 host proteins targeted by SARS-CoV-2 and over 200 perturbed host proteins. The non-structural proteins nsp9 and nsp10 were found to interact with NF-КB repressor NKRF, potentially contributing to the strong inflammatory response and chemotaxis of neut

The passage discusses the findings from a study using single-cell RNA-sequencing and proteomics to compare immune cell composition and activation in mild and severe cases of COVID-19. In mild cases, there was an increase in HLA-DR high CD11c high inflammatory monocytes with an IFN-stimulated gene signature. In contrast, severe cases showed evidence of emergency myelopoiesis, characterized by the presence of immun

The passage discusses the role of hyperglycemia and ACE2 in the severity of COVID-19 infection. The concentration of glycosylated SARS-CoV-2 viral particles and ACE2 in the lung epithelium, as well as the pulmonary immune response to the spike protein around day 8-10 after symptom onset, may determine the disease's severity. Prolonged uncont

The COVID-19 pandemic presents unique challenges in managing patients with cardiovascular risk factors or diseases due to the potential cardiovascular complications. These complications can result from direct viral injury and inflammatory and thrombotic responses to the infection. Proper care of COVID-19 patients requires focused attention on their cardiovascular systems to improve outcomes.

Patients with SARS-CoV-2 infections experience immune system changes and inflammatory cytokine storms, leading to multi-organ damage. The NF-kappa-B pathway, which is induced by several mediators, plays a significant role in cytokine storm. Diabetic patients have a higher risk for COVID-19 due to increased virus entry, impaired immunity response, less viral elimination, and dysregulated

The passage discusses the role of the endothelium in the pathogenesis of Coronavirus Disease 2019 (COVID-19). The endothelium, a crucial part of blood vessel walls, may be involved in the disease's susceptibility and progression. The virus, which invades cells by binding to angiotensin-converting enzyme 2, can gain access to the systemic circulation by infecting or passing

The passage discusses the role of the endothelium in the pathogenesis of Coronavirus Disease 2019 (COVID-19). The endothelium, a crucial part of blood vessel walls, may be a linchpin in COVID-19 susceptibility and complications. The virus, which invades cells by binding to angiotensin-converting enzyme 2, can gain access to the systemic circulation by infect

The SARS-CoV-2 virus, which causes COVID-19, has rapidly spread around the world, affecting over 500,000 people and resulting in over 21,000 deaths as of March 25, 2020. The virus has shown an exponential growth in large countries like China, Europe, and the USA. Older adults and those with underlying medical conditions are particularly vulnerable to the virus. This article discuss

The COVID-19 pandemic poses challenges in managing patients with cardiovascular risk factors or diseases due to the cardiovascular complications observed in patients with the infection. These complications result from direct viral injury and inflammatory and thrombotic responses to the infection. Proper care of COVID-19 patients requires focused attention on the cardiovascular system to improve outcomes.

A 53-year-old female with COVID-19 infection and refractory hypoxemia underwent veno-venous extracorporeal life support (VV-ECLS) and cytokine hemofiltration using a high-cutoff filter. Inflammatory markers improved, leading to decannulation. This is the first reported case of cytokine hemofiltration for COVID-19

Severe COVID-19 caused by SARS-CoV-2 can lead to respiratory failure and ARDS, which results from dysregulated hyperinflammation and NLRP3 inflammasome activation. This pathway triggers the release of proinflammatory cytokines IL-6 and IL-1β. The literature suggests targeting NLRP3 inflammasome as a potential treatment for severe COVID-19.

The passage discusses the role of Angiotensin-converting enzyme 2 (ACE2) in inflammatory lung disease. The text explains that inflammation, triggered by infectious or non-infectious factors, can lead to inflammatory diseases like inflammatory lung disease. The renin-angiotensin system (RAS), including ACE2, has been proposed to contribute to the pathogenesis of inflammat

Interleukin-6 (IL-6), an inflammatory cytokine, plays a role in immune responses to coronaviruses, including COVID-19. IL-6 contributes to cytokine storm, causing inflammation-induced lung injury and multi-organ failure. Research focuses on targeting IL-6 and its receptors as potential therapeutic tactics for COVID-19 based on previous experience with other disorders. This review

The SARS-CoV-2 virus, which causes COVID-19, has been linked to potential impacts on male fertility. The virus enters host cells through the ACE2 receptor, which is expressed in testicular cells. Enhanced testosterone levels may trigger the pathogenesis of COVID-19, but some cases have also reported hypogonadism. Uncontrolled inflammatory responses and resulting oxidative stress from COVID-19

Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by small airway inflammation and irreversible airflow limitation, leading to exacerbations, hospitalization, and increased mortality. About 50% of COPD exacerbations are linked to respiratory viral infections, which can worsen lung function decline and increase hospitalization duration. This article discusses the cellular and molecular mechanisms of virus-induced

A 45-year-old male patient with COVID-19 went through three clinical phases of the disease with distinct manifestations and prognosis. He first presented with fever and pharyngodynia in early April 2020, and was later admitted to a COVID hospital with mild interstitial pneumonia. He was treated with a combination of hydroxychloroquine, ritonavir, darunavir, azithromy

The passage discusses the replication of coronaviruses, specifically SARS-CoV-2, in host cells and the resulting inflammatory consequences. The proposal is made for the use of anti-inflammatory and antiviral prostaglandins as a potential therapy for COVID-19, as they may restrict viral replication and prevent inflammatory responses in the lungs and vital organs. The combination of these prostaglandins with inter

Since late April 2020, there has been an increase in reports of Kawasaki-like syndrome and hyperinflammatory response in children linked to COVID-19. This condition, known as Multisystem Inflammatory Syndrome in Children (MIS-C), is rare and its risk factors, causes, prognosis, and treatment are not yet fully understood. Early recognition is crucial but no standardized treatment guidelines exist. International collaboration will

Chronic obstructive pulmonary disease (COPD) is characterized by inflammation of the lower airways. This inflammation leads to the increased expression of a range of proteins, including cytokines, chemokines, growth factors, enzymes, adhesion molecules, and receptors. Many of these proteins are not typically expressed in normal cells but are induced during inflammation in a cell-specific manner. Transcription factors regulate

The passage aims to analyze the potential mechanisms of cardiovascular dysfunctions caused by COVID-19 and to evaluate effective therapeutic pathways for patients with cardiovascular diseases. COVID-19 primarily damages the lungs but also contributes to hypertension and myocardial damage through various means, including the renin-angiotensin system imbalance, inflammatory storm, hypoxemia, and stress response. Close attention should be paid to both lung and

COVID-19, caused by the novel agent SARS-CoV-2, became a pandemic and major public health concern, leading to social and economic issues. The disease begins when the virus binds to ACE2 receptors and triggers an excessive immune response, resulting in a cytokine storm and organ damage. Genetic polymorphism's effect on the disease course and severity is not yet proven. The clinical course ranges from mild to severe,

COVID-19, caused by SARS-CoV-2, became a pandemic and major public health concern, leading to social and economic issues. The disease begins when the virus binds to ACE-2 receptors and triggers an excessive immune response, resulting in a cytokine storm and organ damage. The role of genetic polymorphism in disease severity is unproven. Clinical presentations range from mild to severe, with older adults and those

Mitochondria, once ancient bacteria, play a crucial role in immune responses to viral infections through interactions between metabolic pathways and inflammatory signals. This commentary discusses how mitochondrial machinery participates in immune responses, mediates antiviral immunity, and is manipulated by viruses to evade it. Additionally, it explores the regulation of mitochondrial machineries in antiviral therapeutics and the challenges and

A study used iAT2s, human lung alveolar type 2 cells derived from induced pluripotent stem cells, to simulate the initial apical infection of the distal lung epithelium with SARS-CoV-2. The results showed that SARS-CoV-2 infection led to a rapid shift to an inflammatory phenotype, with the secretion of cytokines and delayed interferon responses. Over

A study was conducted using the UK Biobank sepsis cohort as a surrogate to identify sepsis-associated genes and correlate them with COVID-19 patients. Sepsis, a life-threatening inflammatory condition with a mortality rate of approximately 20%, shares similar risk factors with severe COVID-19 patients, including severe hypoxia, low platelet count, elevated bilirubin, hypoalbum

The passage discusses the activation of natural killer (NK) cells in COVID-19 patients based on a study using 28-color flow cytometry and single-cell RNA sequencing. The researchers identified distinct immunophenotypes of NK cells in peripheral blood, which were linked to disease severity. These immunophenotypes were characterized by high expression of perforin, NKG2C, and Ksp37, indicating

A study examining mHLA-DR expression, a marker of innate immune suppression, in critically ill COVID-19 patients admitted to the ICU found no indications of overt innate immune suppression. The patients, who were all mechanically ventilated and had high levels of inflammatory markers, displayed mostly normal mHLA-DR expression levels that did not change over time. Despite a pronounced inflammatory response, none of the COVID

Researchers conducted a comprehensive analysis of gene expression data from the blood, lung, and airway of COVID-19 patients to better understand the host response to SARS-CoV2 and identify potential therapeutic targets. Results indicate COVID-19 pathogenesis is driven by inflammatory myeloid-lineage cells with distinct signatures in each compartment. The relative absence of cytotoxic cells in the lung suggests delayed virus clearance may contribute to disease

COVID-19, caused by SARS-CoV-2, has led to a global pandemic and is associated with significant organ dysfunction syndrome, including cardiovascular impairment. Cardiovascular protective strategies are crucial for COVID-19 patients. Mechanisms of cardiovascular impairment include direct viral infection, cytokine storm, and aggravation of existing cardiovascular diseases, all of which are driven by hyperactivated inflammation. Anti

A study explores the sex differences in COVID-19 patients, with men having a higher risk of severe cases and higher fatality rates. Factors such as hormonal levels and immune functions are considered in understanding these differences. The study reviews reports on how sex affects ACE2, a key component in COVID-19 pathogenesis, and summarizes gender differences in immune responses and the role of sex hormones in immune processes. Additionally, the study examines available data on the

A significant number of COVID-19 patients experience hepatic injury, particularly those with severe or critical illness. The main pathologic changes include sinusoidal lymphocytic infiltration and multifocal hepatic necrosis. Both direct viral-induced cellular injuries and potential hepatotoxicity from therapeutic drugs are possible causes. Additionally, preexisting chronic liver disease and COVID-19-related hyper-

Multiple sclerosis (MS) is an inflammatory disease causing damage to myelin sheaths in the brain and spinal cord, leading to demyelination, scarring, and various symptoms. Autoimmune response to self-antigens in genetically susceptible individuals triggers the disease, with T cells, particularly T(H)1 and T(H)17 subsets, playing a significant role. Regulatory T cells (T

Mönkemüller et al. discussed the pathogenesis of COVID-19 in the gastrointestinal tract, emphasizing the local and systemic inflammatory response caused by SARS-CoV-2. They reported three cases of severe colonic ischemia and elevated D-dimer levels in COVID-19 patients with severe acute respiratory distress syndrome. The authors highlighted the thromboembolic complications in COVID-

This passage discusses four cases of delirium caused by COVID-19 infection in older patients with cognitive decline. Unique features of the delirium included rigidity, alogia, abulia, and elevated inflammatory markers. In three of the cases, mental status change was the presenting symptom without significant respiratory symptoms. Possible explanations for COVID-19 delirium include primary CNS invasion by the virus or secondary enceph

Filoviruses, including ebolavirus and marburgvirus, infect and target antigen-presenting cells (APCs), particularly macrophages and dendritic cells, during hemorrhagic fever. The mechanisms behind these interactions, including filovirus replication in different APC subsets, cellular signaling pathways leading to cytokine and chemokine production, and innate antiviral response disabling, remain unclear. A

The passage discusses the urgent need for pharmacological agents or vaccines to treat Coronavirus Disease 2019 (COVID-19), caused by SARS-CoV-2. While several agents are under investigation, no approved treatment exists. The disease's pathogenesis involves excessive inflammatory and immune response, as well as oxidative injury. This review focuses on updating the knowledge about COVID-19's pathogenesis,

The passage discusses the urgent need for pharmacological agents or vaccines to treat and prevent Coronavirus Disease 2019 (COVID-19), caused by SARS-CoV-2. While several agents are under investigation, no approved treatment exists. The disease's pathogenesis involves excessive inflammation, immune response, and oxidative injury. This review focuses on updating the knowledge about COVID-19's pathogenesis, clinical

The passage discusses Theiler's murine encephalomyelitis virus (TMEV) as a model for understanding multiple sclerosis, a demyelinating disease. While virus-specific Th1 and cytotoxic T cell (CTL) responses are primarily protective against the disease, Th1 responses to myelin antigens contribute to demyelination. Cytokine production in the central nervous system (CNS) during the disease process supports

COVID-19 causes multiorgan damage beyond the lungs in severe cases, leading to increased risk of death from kidney injury. The inflammatory response, not the virus itself, causes tissue injury through hypercytokinemia and aggressive inflammation. The complement system, the first response to SARS-CoV-2 infection, contributes to acute and chronic inflammation, endothelial cell dysfunction, thrombus formation, and intrav

COVID-19 causes multiorgan damage beyond the lungs in severe cases, leading to increased risk of death from cardiac injury and acute kidney injury. The inflammatory host immune response, not the virus itself, causes tissue injury through hypercytokinemia and aggressive inflammation. The complement system, which is the first response of the immune system to SARS-CoV-2 infection, contributes to acute and chronic inflammation, endot

A study was conducted to investigate the role of vitamin E acetate (VEA) and medium-chain triglycerides (MCT) in e-cigarette-associated lung injury (EVALI). The study found that exposure to these substances and e-cigarette vape cartridges led to oxidative damage, inflammatory responses, and cytotoxicity in pulmonary epithelium and immune cells. In

SARS-CoV-2 infects monocyte-derived dendritic cells (moDCs) and macrophages (MDMs), leading to an attenuated interferon response and significant pro-inflammatory cytokine/chemokine expression in MDMs but not in moDCs. This attenuated immune response in moDCs is associated with viral antagonism of STAT1 phosphorylation, which may

The passage discusses the immunological and inflammatory profiles of mild and severe COVID-19 cases. Severe cases have more pronounced lymphopenia, selective loss of CD4+ T cells, CD8+ T cells, and NK cells, excessive T-cell activation, and high expression of T-cell inhibitory molecules. CD8+ T cells in severe cases express high levels of cytotoxic molecules. Lung tissue from a fat

COVID-19 infection can range from asymptomatic to severe, with some cases leading to macrophage activation syndrome and cytokine storm syndrome. Factors contributing to severe disease and cytokine storm include impaired SARS-CoV-2 clearance, lower interferon levels, increased neutrophil extracellular traps, and genetic mutations. Once immunologic complications occur, anti-viral treatment should be combined with

A study on SARS-CoV-2 explores its genome sequence similarities to SARS-CoV and MERS-CoV, but the emergence of the new virus has rendered existing drugs ineffective. The research focuses on analyzing potential drug target proteins, mutations, genetic diversity, and pathogenicity of SARS-CoV-2. Structural analysis of drug target proteins provides insights into their mechanism of pathogenesis and structure-

The passage discusses the emergence of SARS-CoV-2 and its close relationship to SARS-CoV and MERS-CoV, but the ineffectiveness of existing drugs against it. The review examines genetic differences, mutations, and structural analysis of potential drug target proteins in SARS-CoV-2, as well as differences in cytokine profiling and inflammatory signaling. Minimal genome sequence variation may

The passage discusses two mutant murine coronaviruses with different interferon antagonists: one with reduced deubiquitinase (DUB) activity (DUBmut) and the other with inactivated endoribonuclease (EndoU) activity (EndoUmut). The DUBmut virus activates an earlier interferon response but has similar replication kinetics and pathogenesis as the wild type virus. In contrast,

Eosinophils, discovered over 140 years ago, are polymorphonuclear leukocytes with active metabolism and intracellular secretory granules. Classically linked to type 2 immune responses against parasites and allergies, eosinophils also play a role in host protection against fungi, bacteria, and viruses. They release cationic proteins, cytokines, chemokines, and other molecules

Ebola virus is a highly virulent pathogen that causes hemorrhagic fever syndrome by subverting both innate and adaptive immune responses and triggering harmful inflammatory responses. The virus overwhelms the host immune system, leading to cell damage in the liver and vasculature, often resulting in death from septic shock. Future research will focus on understanding interspecies transmission, molecular mechanisms of pathogenesis, and protective immune responses to Ebola virus.

This study investigates the role of decoy receptor 3 (DcR3) in Hemorrhagic fever with renal syndrome (HFRS), a viral disease characterized by fever, hemorrhage, and renal failure. The researchers found that serum DcR3 levels significantly increased during the oliguric phase and in the critical group, and were closely related to pro-inflammatory cytokines and kidney injury markers

This study investigated the expression of inflammation-related genes in the lungs of BALB/c mice infected with two strains of H7N9 influenza A virus, which differed only in the PB2 residue 627. The results showed that NLRP3, RIP3, IL-1β, and TNF-α had significantly higher expression levels in H7N9-infected groups, contributing to lung pathological lesions.

The passage discusses the role of pathogenic CD4+ T cells and inflammatory monocytes in the severe lung pathology and high mortality observed in COVID-19 patients. After SARS-CoV-2 infection, CD4+ T cells become pathogenic Th1 cells, generating cytokines that induce inflammatory monocytes with high IL-6 expression. These cells enter the pulmonary circulation in large numbers, contributing

The COVID-19 outbreak, causing significant mortality and health concerns in over 150 countries, has hindered the identification of effective therapeutic drugs due to limited knowledge of the host immune response. To address this, transcriptome sequencing was performed on RNAs from bronchoalveolar lavage fluid (BALF) and peripheral blood mononuclear cells (PBMC) of COVID-19 patients. Results showed distinct cytokine profiles

The COVID-19 outbreak, causing significant mortality and health concerns in over 150 countries, has hindered the identification of effective therapeutic drugs due to limited knowledge of the host immune response. To address this, transcriptome sequencing was performed on RNAs from COVID-19 patients' bronchoalveolar lavage fluid and peripheral blood mononuclear cells. Results showed distinct cytokine profiles in response to SARS-CoV

This study aimed to identify distinct bronchoalveolar lavage lipidome profiles in community-acquired pneumonia (CAP) patients using untargeted lipidomic profiling analysis and clustering methods. Principal component analysis (PCA) and partitioning clustering analysis (k-means) were employed to evaluate variations and potential clusters. Results showed significant differences in BALF lipidomes between CAP and control groups, with lactosylcer

The passage discusses the role of inflammation in infectious diseases and how altered inflammatory responses can lead to disease progression. It introduces the concept of resolution mediators, which decrease inflammation and enhance the host's ability to fight infection. In the context of COVID-19, the article suggests that pro-resolving mediators could be beneficial in treating late-stage disease due to their anti-inflammatory, anti-thrombogenic

The passage discusses the role of inflammation in infectious diseases, including COVID-19, and the importance of endogenous mediators that drive inflammation resolution. These mediators decrease inflammatory responses and enhance the host's ability to combat infection. In the lung, pro-resolution molecules or strategies that promote their increase suppress inflammation and lung injury, and facilitate control of viral or bacterial burden. The passage suggests that the anti-infl

Microglia, the resident macrophages of the brain, play a protective role in viral encephalitis by coordinating the innate immune response to viral infection. Depletion of microglia in mouse models leads to increased viral replication, more severe neurological disease, and heightened mortality. Mechanisms include microglial interactions with T cells and phagocytosis of infected neurons. Inflammatory cytokine production

Patients with heart failure are more susceptible to COVID-19 and experience more severe symptoms. Myocardial injury, indicated by increased troponin levels, occurs in up to 35% of hospitalized COVID-19 patients, particularly those who are critically ill or have concurrent cardiac disease. Mechanisms contributing to myocardial injury include fever, tachycardia, adrenergic stimulation, inflammation, and endotheliitis

A study explored the role of neuropilin-1 (NRP1) in the inflammatory response of blood-brain barrier (BBB) endothelial cells, which is crucial in central nervous system inflammatory diseases like multiple sclerosis. Knockdown of NRP1 in brain microvascular endothelial cells suppressed IFNγ-induced C-X-C motif chemokine 10 expression and STAT

A 75-year-old stage-III NSCLC patient underwent radio-chemotherapy and durvalumab treatment, but developed pneumonitis and had immunotherapy suspended. After four cycles, he suddenly developed fever and severe dyspnea, with chest radiography showing diffuse alveolar and interstitial infiltrates. RT-PCR confirmed Covid-19 diagnosis, but his condition worsened despite antiviral therapy and

The COVID-19 pandemic caused by SARS-CoV-2 has been linked to liver dysfunction in some patients, with elevated serum aspartate aminotransferase levels. The cause of this liver damage is unclear, with potential contributing factors including viral infection, use of hepatotoxic drugs, systemic inflammation, respiratory distress, and multiple organ dysfunction. This review article examines the demographic and clinical characteristics

The passage discusses a study examining host transcriptomes in moderate and severe COVID-19 cases to identify pathways affecting disease progression. Differentially regulated genes (DEGs) were categorized into cellular pathways, with the majority related to immune activation, cytokine signaling, pathogen uptake, host defenses, blood and vasculature genes, and SARS-CoV-2- and other virus-affected path

Crimean Congo hemorrhagic fever virus (CCHFV) causes a potentially fatal disease with symptoms including fever, myalgia, hemorrhages, raised liver enzymes, and increased bleeding markers. The virus, prevalent in about 30 countries, employs mechanisms to avoid triggering antiviral type I interferons. Recent studies have suggested a role for inflammatory cytokines in the disease's pathogenesis

The passage discusses the COVID-19 pandemic caused by the SARS-CoV2 virus, which shares similarities with past coronaviruses and can lead to respiratory symptoms and acute respiratory distress syndrome. The management of COVID-19 includes ventilatory support, broad-spectrum antiviral drugs, and vaccines, which have not been developed yet. Some anti-rheumatic drugs, such as antimalarials, anti-

A study using single-cell RNA sequencing on nasopharyngeal and bronchial samples from patients with moderate or critical COVID-19 and healthy controls identified epithelial cell types and states vulnerable to SARS-CoV-2 infection. Patients with severe COVID-19 showed an average three-fold increase in ACE2 expression, which correlated with interferon signals by immune cells. Critical cases exhibited stronger interactions between epithel

A study using single-cell RNA sequencing on nasopharyngeal and bronchial samples from patients with moderate or critical COVID-19 and healthy controls identified epithelial cell types and states vulnerable to SARS-CoV-2 infection. Patients with severe COVID-19 showed an average three-fold increase in ACE2 expression, which correlated with interferon signals by immune cells. Critical cases had stronger interactions between epithelial

The human Respiratory Syncytial Virus (hRSV) is the leading cause of severe acute lower respiratory tract infections in humans, and vaccination with formalin-inactivated hRSV (FI-hRSV) has resulted in disease exacerbation due to the formation of immune complexes (hRSV-ICs) and engagement of Fc gamma receptors (FcγRs) on immune cells.

The passage discusses the connection between COVID-19 and cancer, with a focus on the increased risk of severe disease progression in cancer patients and the potential for SARS-CoV-2 to contribute to cancer development. The interplay of the inflammatory immune response and tissue damage caused by COVID-19 infection is also explored. Research on the long-term consequences of COVID-19, including the possibility of cancer development, is emphasized.


Question: What is the mechanism of cytokine storm syndrome on the COVID-19?

The passage discusses the impact of coronavirus disease 2019 (COVID-19) on patient safety and social stability, with some severe cases leading to acute respiratory distress syndrome or multiple organ failure. The primary cause of disease deterioration is cytokine storm. Current treatments, including interleukin-6 antibody blockers, stem cell therapy, and convalescent plasma transfusions, have shown progress in counteracting cyt

COVID-19, caused by the Corona Virus, has led to significant health and social issues, with some patients developing acute respiratory distress syndrome or multiple organ failure in later stages. A major contributing factor to this deterioration is the cytokine storm mechanism. Current treatments, including interleukin-6 antibody blockers, stem cell therapy, and convalescent plasma transfusions, have shown progress in counteracting the cytokine

A 48-year-old male with severe COVID-19 was treated with tocilizumab, an IL-6 receptor inhibitor, to prevent a cytokine storm and avoid mechanical ventilation. The patient's declining respiratory status and increasing acute phase reactant levels indicated the potential onset of a cytokine storm. The treatment was well-tolerated and the patient experienced improvements in respiratory symptoms and clinical status.

The passage discusses the possible mechanism behind the cytokine storm in elderly adults with COVID-19 infection. The severity of COVID-19 infections varies widely, with elderly adults experiencing deadly critical cases and cytokine storms, which can lead to edematous ARDS, pneumonia, and multiple organ failure. The reason for this is unclear, but it is believed that aging, or "inflamm-aging," which is characterized by mildly elev

Tocilizumab, a humanized monoclonal antibody, is used to treat CRS or cytokine storm syndrome in severe COVID-19 patients by binding to both membrane-bound and soluble IL-6 receptors and inhibiting the JAK-STAT signaling pathway. More research is needed to understand the molecular mechanism of tocilizumab's activity.

A novel coronavirus pneumonia (COVID-19) outbreak, causing severe pneumonia in 15.7% of patients and rapid disease progression due to cytokine storm, has no specific treatment. IL-6, a key cytokine in infection-induced cytokine storm, is targeted by Tocilizumab, an IL-6 receptor antagonist approved for cytokine release syndrome (CRS)

COVID-19 infection can range from asymptomatic to severe, with some cases leading to macrophage activation syndrome and cytokine storm syndrome. Factors contributing to severe disease and cytokine storm include impaired SARS-CoV-2 clearance, lower interferon levels, increased neutrophil extracellular traps, and genetic mutations. Once immunologic complications occur, anti-viral treatment should be combined with

A novel coronavirus, SARS-CoV-2, causing COVID-19, leads to severe pneumonia, acute lung injury, acute respiratory distress syndrome, and multiple organ dysfunction syndrome. Immune over-activation resulting in a cytokine storm contributes to deaths in late stages of the disease. The mechanisms of SARS-CoV-2-induced cytokine storm are reviewed, with suggestions for targeted cyt

COVID-19, a global pandemic causing respiratory infection, leads to pneumonia and acute respiratory distress syndrome (ARDS) in some cases. Mortality is linked to the "cytokine storm" caused by excessive production of proinflammatory cytokines, leading to ARDS aggravation, multi-organ failure, and death. Targeting cytokines during treatment could improve survival and reduce mortality.

COVID-19, caused by SARS-CoV-2, has become a global pandemic with over 4 million confirmed cases as of May 11, 2020. The virus primarily spreads through respiratory droplets and close contact. Clinical data indicates that a cytokine storm contributes to COVID-19 severity and mortality. With no antivirals or vaccines available, understanding the cytokine storm in

A cancer survivor with COVID-19 developed acute respiratory failure due to a cytokine storm. Despite treatment with hydroxychloroquine, azithromycin, and ceftriaxone, the patient remained critically ill and required mechanical ventilation. He was later treated with tocilizumab, which led to improvement and successful extubation, suggesting a potential role for tocilizumab in managing cytokine storm in

COVID-19, caused by SARS-CoV-2, is a global health threat with over 290,000 deaths. Symptoms range from mild to severe pneumonitis and ARDS. Severe cases experience immune overactivation, or a cytokine storm, which can lead to multiple organ failure and death. This review covers COVID-19 epidemiology, SARS-CoV-2-induced cyt

The lung is a primary target of the cytokine storm caused by SARS-CoV-2, leading to COVID-19. This dysregulated immune response damages alveolar epithelial and vascular endothelial cells, causing lung infiltration by neutrophils and macrophages. IL-6 and other cytokines/chemokines contribute to this inflammatory response. Targeting cytokines, their

The passage discusses the immune response and immunopathological changes in COVID-19, a disease caused by the SARS-CoV-2 virus. Asymptomatic cases are common, but many patients experience a self-limiting viral respiratory disease. Neutralizing antiviral T cell and antibody immunity develops after infection. Severe cases exhibit unique features such as severe lymphopenia and eosinopenia, extensive

The passage discusses the immune response and immunopathological changes in COVID-19, which is currently a global pandemic. Asymptomatic cases are common, and most patients experience a self-limiting viral respiratory disease. However, high viral load and repeated exposure can lead to severe disease, including lymphopenia, eosinopenia, extensive pneumonia, lung damage, cytokine storm, acute respiratory distress syndrome

Patients with severe COVID-19 may experience a cytokine storm, characterized by an excessive release of inflammatory cytokines. The cause is believed to be the attachment of the SARS-CoV-2 spike protein to the angiotensin-converting enzyme 2 (ACE2) receptor, leading to hyperinflammation. Four molecular axes contributing to this inflammatory response are discussed: the renin

The passage discusses the role of cytokine storm and leukocyte changes in severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection, specifically in the context of 3939 COVID-19 patients in China. The text indicates that severe cases of COVID-19 result in alveolar injury and multi-organ failure, which are associated with hyperproduction of cytokines. Both mild and

The passage discusses the role of cytokine storm and leukocyte changes in severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection, specifically in the context of 3939 COVID-19 patients in China. The text explains that severe COVID-19 outcomes are often due to alveolar injury and multi-organ failure, which are associated with hyperproduction of cytokines. Both mild

A novel coronavirus, SARS-CoV-2, causing COVID-19 was identified in December 2019 and spread rapidly worldwide. The virus enters cells through the angiotensin-converting enzyme II (ACE2) receptor. COVID-19 is characterized by a sudden deterioration of disease, low lymphocyte levels, and high pro-inflammatory cytokines. Severe cases experience cyt

The passage discusses the progression of COVID-19 to severe or critical illness, which is often associated with cytokine storm, indicated by elevated serum levels of certain cytokines. The article summarizes previous research on using Traditional Chinese Medicines (TCM) to treat severe cases of SARS, focusing on those targeting cytokine storm. Data mining and network pharmacology were used to investigate the mechanisms and pathways involved in TCM

The passage discusses the background of COVID-19 and its severe forms characterized by acute respiratory distress syndrome (ARDS) and multiple-organ failure (MOF). The pathophysiology of COVID-19 is not fully understood, and effective treatments are lacking. The cytokine storm, or excessive cytokine release in response to viral infection, is believed to be the mechanism leading to ARDS and MOF. The article aims to explore potential

The passage discusses the potential use of Jaktinib hydrochloride in treating cytokine storms in patients with COVID-19. SARS-CoV-2 infection, caused by the coronavirus, is a major public health threat and is known to cause cytokine storms, which can worsen the condition from mild to severe or critical. Current treatments for cytokine storms are limited, and there is a focus on finding an

Pirfenidone, an anti-fibrotic agent with minimal side effects, could be a potential treatment for COVID-19. Approved for mild to moderate Idiopathic Pulmonary Fibrosis, pirfenidone inhibits apoptosis, downregulates ACE receptors expression, decreases inflammation, and ameliorates oxidative stress. These mechanisms could protect pneumocytes and other cells from COVID-19 invasion

The passage suggests that COVID-19 can lead to mortality in some patients due to a condition called cytokine storm syndrome. To mitigate this, the authors propose IL-6 receptor (IL-6R) antagonist therapy for COVID-19 patients. Two humanized monoconal antibodies, tocilizumab and sarilumab, are currently in clinical trials for this purpose. However, researchers and physicians are encouraged to explore additional IL

Two COVID-19 patients with severe pneumonia and acute respiratory distress syndrome (ARDS) recovered after receiving tocilizumab, a treatment proposed for cytokine storm syndrome caused by hyperactive immune systems. Both patients had previously responded to antiviral therapy. This case suggests tocilizumab's effectiveness in treating COVID-19-related ARDS, but further studies are needed to assess its safety and efficacy.

A retrospective study of 568 critically ill COVID-19 patients in Wuhan's Tongji Hospital found that those who received hydroxychloroquine (HCQ) had a lower mortality rate (18.8%) compared to those who did not receive HCQ (45.8%). The HCQ group also had a shorter hospital stay and lower levels of inflammatory cytokine IL-6 at the

The passage suggests that COVID-19 leads to mortality in some patients due to a condition called cytokine storm syndrome. To mitigate this, the authors propose IL6 receptor antagonist therapy for COVID-19 patients. Two humanized monoclonal antibodies, tocilizumab and sarilumab, are currently in clinical trials for this purpose. However, researchers and physicians are encouraged to explore additional IL6 receptor antagonists to

The passage discusses the potential use of the flavonolignan silibinin as a treatment for COVID-19, the illness caused by the novel coronavirus SARS-CoV-2. Silibinin is suggested to target both the host's inflammatory response and the virus replication machinery. As a direct inhibitor of STAT3, a regulator of inflammatory cytokine signaling, silibinin may limit c

The passage discusses the correlation between poor outcomes in COVID-19 and cytokine storm syndrome. It suggests that broad screening for cytokine storm and early anti-inflammatory therapy could prevent immunopathology and help conserve healthcare resources. The authors recommend learning from clinical experience in cytokine storm syndromes to benefit teams treating severe COVID-19 patients.

The passage discusses the correlation between poor outcomes in COVID-19 and cytokine storm syndrome. It suggests that broad screening for cytokine storm and early anti-inflammatory therapy could prevent immunopathology and help conserve healthcare resources. The authors recommend drawing from clinical experience in managing cytokine storm syndromes to improve care for severe COVID-19 patients.

A 55-year-old patient with primary myelofibrosis, significant comorbidities, and a 15-month history of ruxolitinib treatment experienced stable COVID-19 pneumonia without the need for mechanical ventilation or vasopressors. Continuation of ruxolitinib treatment prevented cytokine storm and ARDS.

A 55-year-old patient with primary myelofibrosis, significant comorbidities, and a 15-month history of ruxolitinib treatment experienced stable COVID-19 pneumonia without the need for mechanical ventilation or vasoppressors. Continuation of ruxolitinib treatment prevented cytokine storm and ARDS.

The passage discusses COVID-19, also known as the severe acute respiratory syndrome novel coronavirus disease. When severe, COVID-19 is a systemic illness marked by hyperinflammation, cytokine storm, and increased cardiac injury biomarkers. The article reviews the current understanding of COVID-19's pathophysiology, cardiovascular manifestations, and potential treatments, providing a comprehensive overview up to April 3,

The passage summarizes a article about the cytokine storm, an excessive immune response leading to high mortality. During the COVID-19 epidemic, some severe cases have been linked to this condition. The article aims to explain the mechanisms behind COVID-19-induced inflammatory storm and propose treatment strategies.

The passage discusses the cytokine storm, an extreme immune response to external stimuli, and its connection to high mortality in COVID-19 patients. The article aims to provide insight into the mechanisms behind COVID-19-induced inflammatory storms and potential treatment strategies.

The SARS-CoV2 infection caused by COVID-19 leads to different clinical phenotypes based on the amount of cytokines released. Mild cases have a balanced cytokine response, severe cases experience a cytokine storm leading to lung damage, and critical cases have an uncontrolled immune response resembling secondary hemophagocytic lymphohistiocytosis, resulting in multi-organ failure. An immune-modul

The SARS-CoV2 infection caused by COVID-19 leads to different clinical phenotypes based on the amount of cytokines released. Mild cases have a balanced cytokine response, severe cases experience a cytokine storm leading to lung damage, and critical cases have an uncontrolled immune response resembling secondary hemophagocytic lymphohistiocytosis, potentially resulting in multi-organ failure. An immune-mod

A subset of COVID-19 patients experience cytokine storm syndrome (CSS) with elevated inflammatory cytokines, particularly interleukin-6 (IL-6). The success of IL-6 receptor blockade in treating CAR T-cell therapy-related CRS has led to investigations of using tocilizumab for COVID-19 CSS.

A subset of COVID-19 patients experience cytokine storm syndrome (CSS) with elevated inflammatory cytokines, particularly interleukin-6 (IL-6). The success of IL-6 receptor blockade in treating CAR T-cell therapy-related CRS is leading to investigations of using tocilizumab for COVID-19 CSS.

The passage discusses the complex relationship between COVID-19 and the cytokine storm, which can lead to secondary haemophagocytic lymphohistiocytosis (sHLH). While some COVID-19 patients develop fully blown sHLH, others exhibit features of hyperinflammation without meeting sHLH criteria. The cause of sHLH varies, and the differences lie in the phases of the process. The discovery of a hyperinflam

The passage discusses the complex relationship between COVID-19 and the cytokine storm, which can lead to secondary haemophagocytic lymphohistiocytosis (sHLH). While some COVID-19 patients develop fully blown sHLH, others exhibit features of hyperinflammation without meeting sHLH criteria. The cause of sHLH varies, and the differences lie in the various phases of the process. The identification of a hyperinfl

The passage discusses the limited knowledge on the immune status of COVID-19 patients and the importance of understanding it by referencing previous coronaviruses, SARS-CoV and MERS-CoV. Elevated pro-inflammatory cytokines and dysregulated interferon-1 response in COVID-19 patients are similar to SARS and MERS, suggesting a possible cytokine storm-mediated lung damage. An adapt

A letter by Randy Cron and colleagues drew attention to the connection between the cytokine storm syndrome (CSS) in macrophage activation syndrome common in rheumatology and the CSS proposed to occur in SARS-CoV-2 infection. Amid the virus's high contagion, the scientific community was faced with an infodemia, urgently seeking effective therapies while managing patients.

Hemophagocytic syndrome (HLH), also known as hemophagocytic lymphohistiocytosis, is a severe inflammatory disorder characterized by cytopenia, excessive cytokine production, and hyperferritinemia. Common symptoms include fever, lymphadenopathy, hepatosplenomegaly, and multiorgan failure. HLH can have primary (genetic) or secondary (re

The passage discusses the disproportionate impact of severe COVID-19 and deaths in older adults, and argues that monocytes, a type of circulating immune cell, play a key role in the cytokine storm and associated pathologies in COVID-19. Monocyte function and phenotype changes in both aging and severe COVID-19, suggesting a potential mechanism for increased morbidity and mortality in older adults. The innate immune system is

The passage discusses COVID-19, the illness caused by the novel coronavirus SARS-CoV-2. Severe cases of COVID-19 involve systemic symptoms including hyperinflammation, cytokine storm, and increased cardiac injury biomarkers. This review covers the underlying causes of COVID-19, its cardiovascular effects, and potential treatments, providing a comprehensive overview up to April 3, 2020.

The passage discusses the role of catecholamines and cytokines in the severity and mortality of COVID-19, specifically in the context of a cytokine storm syndrome (CSS). The study suggests that catecholamines enhance inflammatory injury by increasing IL-6 production through alpha-1 adrenergic receptor (α1-AR) signaling. Prophylactic inhibition of catecholamine synt

The passage presents a hypothesis suggesting that the low molecular weight fraction of commercial human serum albumin (LMWF5A), a novel biologic being developed for osteoarthritis, could improve clinical outcomes of COVID-19 by attenuating hyperinflammation and potential cytokine storms. In vitro studies indicate that LMWF5A reduces production of pro-inflammatory cytokines and promotes resolution of inflammation. A

A case is presented of a COVID-19 patient who developed Posterior Reversible Encephalopathy Syndrome (PRES), characterized by typical imaging findings. The inflammatory response to COVID-19 infection is linked to PRES through increased cytokine levels and endothelial injury. Given the widespread COVID-19 pandemic, more cases of PRES are anticipated.

The 2019 Novel Coronavirus Pandemic caused by the SARS-COV2 Virus, also known as COVID-19, which was first reported in China in December 2019, has become a significant global health concern. The virus can lead to cytokine storm, an inflammatory response with excessive production of proinflammatory cytokines, resulting in lung disease and acute respiratory distress syndrome.

The 2019 Novel Coronavirus Pandemic, caused by the SARS-COV2 Virus (COVID-19), initially reported in China in December 2019, is a significant global health concern. The virus can lead to cytokine storm, an inflammatory response causing lung disease and acute respiratory distress syndrome, potentially resulting in septic shock and multi-organ failure. This article provides an overview of the

A hyperinflammatory state, or "cytokine storm," is a severe complication of COVID-19. While several anti-inflammatory/immunosuppressive agents are being evaluated, there is insufficient evidence for their efficacy and safety. The authors suggest that selective inhibition of phosphodiesterase 4 (PDE4), which plays a role in the inflammatory response, may attenuate the cyt

A hyperinflammatory state, or "cytokine storm," is a severe complication of COVID-19. While several anti-inflammatory/immunosuppressive agents are being studied, there is insufficient evidence for their efficacy and safety. The authors suggest that selective inhibition of phosphodiesterase 4 (PDE4) may attenuate the cytokine storm by inhibiting pro-inflammatory

The passage discusses the use of immunotherapies as an adjunct treatment for severely ill COVID-19 patients. With no specific therapies for COVID-19, most patients rely on mechanical ventilation. The early immune response to COVID-19 causes severe lung damage through cytokine storm and immune cell migration to the lungs. Due to uncertainties and potential risks of immunosuppressive treatments like corticosteroids, the authors suggest immun

The passage discusses the use of immunotherapies as an adjunct treatment for severely ill COVID-19 patients. COVID-19, caused by SARS-CoV-2, has infected millions with over 275,000 fatalities as of May 8, 2020. There are currently no specific COVID-19 therapies, and most patients require mechanical ventilation. The early immune response to COVID-19 involves c

The COVID-19 pandemic caused by SARS-CoV-2 has led to a global health crisis, with patients experiencing strong cytokine and interferon production and associated cytokine storm syndrome. The lack of approved therapies or vaccines to treat COVID-19 highlights the need for existing treatments to address hyperinflammation and reduce mortality. This review explores potential options, including antivirals, vaccines, small-molecules,

The COVID-19 pandemic, caused by SARS-CoV-2, leads to acute respiratory distress syndrome (ARDS) and high mortality rates due to an uncontrolled inflammatory response and cytokine storm. Chinese researchers suggest using anti-inflammatory agents as part of the treatment for COVID-19 patients.

The cause of Covid-19-related kidney damage, or Covid-19 nephropathy, is not yet clear and is believed to result from a combination of factors including dehydration leading to pre-renal failure, toxic damage from cytokine storm or rhabdomyolysis, direct damage to kidney cells by the virus, and drug-induced nephrotoxicity.

A multicentre randomized controlled trial is being conducted to investigate the effectiveness and safety of intravenous high-dose vitamin C (HIVC) in treating severe COVID-19 patients with acute respiratory distress syndrome (ARDS) and multiorgan dysfunction. The hypothesis is that HIVC can suppress cytokine storms caused by COVID-19, improve pulmonary function, and reduce the risk of ARDS. The study plans to recruit

The study reveals that inhibiting JAK1 kinase in mice with hypersensitivity to interferon due to overexpression of interferon receptor genes prevents lethal immune responses, cytokine storm, and organ failure.

COVID-19, a contagious disease affecting elderly and comorbid individuals, causes lung injury through a robust immune response leading to cytokine storm. Nicotinamide, a PARP inhibitor, is suggested as a supportive treatment to prevent cytokine storm-induced lung damage. Previously used for reducing lung injury from ventilators and hypoxia, nicotinamide may alter the course of COVID-19. PARP plays a

The COVID-19 pandemic has caused a national emergency in the United States, leading to a high risk for millions of Americans and a shortage of medical resources. The disease can lead to severe illness, including septic shock and multiple organ dysfunction, and currently approved treatments are only supportive. The present cytokine storm caused by an overactive immune system can lead to organ damage, acute respiratory distress syndrome, acute cardiac injury, and secondary infections, potentially resulting

The COVID-19 pandemic has caused a national emergency in the United States, leading to a recession and disrupted lifestyles. The disease can lead to severe illness and death, with high-risk individuals outnumbering available medical resources. Current treatments are supportive but not curative, and new treatments such as vaccines, Remdesivir, hydroxychloroquine, and combination therapy are being studied. Expanded umbilical cord mesenchymal

A severe COVID-19 patient who experienced a cytokine storm and required mechanical ventilation due to ARDS had a poor prognosis. However, their outcome improved after timely intervention with extracorporeal blood purification (EBP).

A subset of severe COVID-19 patients experience inflammation and multi-organ dysfunction similar to Cytokine Storm Syndromes (CSS) such as secondary hemophagocytic lymphohistiocytosis (sHLH), idiopathic multicentric Castleman disease (iMCD), and CAR-T cell therapy associated CRS. Novel cytokine-targeting treatments are the standard for CSS, and this review

A subset of severe COVID-19 patients experience inflammation and multi-organ dysfunction similar to Cytokine Storm Syndrome (CSS). This review compares CSS in COVID-19 to other hematological CSS, including secondary hemophagocytic lymphohistiocytosis (sHLH), idiopathic multicentric Castleman disease (iMCD), and CAR-T cell therapy associated CRS. Novel cyt

A study suggests that overexpression of Kv1.3 channels in lymphocytes leads to overactivation of cellular immunity and cytokine storm in severe cases of COVID-19. Previous research shows that chloroquine and azithromycin suppress Kv1.3 channel activity and cytokine production from lymphocytes. This mechanism could explain the effectiveness of these drugs in treating severe COVID-19 cases.

The SARS-CoV2 virus, responsible for COVID-19, is a highly pathogenic coronavirus that can lead to fatal lower respiratory tract infections and ARDS. The immune response to the virus can result in a "cytokine storm," characterized by high cytokine concentrations, which contributes to lethal symptoms. Individuals with underlying risk factors, such as diabetes, hypertension, cardiovascular disease, and COPD, are

SARS-CoV-2 infection leads to lymphopenia due to the exhaustion and decreasing count of natural killer cells and T cells. This is caused by the body's inability to eradicate the infection, resulting in hyperactivation of the immune system and excessive release of inflammatory cytokines, known as a cytokine storm syndrome. The paper discusses these mechanisms and potential therapeutic targets.

SARS-CoV-2 infection leads to lymphopenia due to exhausted natural killer cells and T cells. The inability to eliminate the virus results in hyperactivation of the immune system, releasing excessive inflammatory cytokines and causing a cytokine storm syndrome. This paper discusses the mechanisms and potential therapeutic targets for addressing lymphopenia in COVID-19.

A new disease caused by the SARS-CoV-2 virus, known as COVID-19, emerged in December 2019. No specific antiviral therapy has been approved for COVID-19. Instead, evidence suggests a hyperinflammatory state or "cytokine storm" in COVID-19 patients, with IL-6 playing a key role in predicting adverse outcomes and mortality. Given the prevalence of comorbidities like

A group of patients with COVID-19 caused by SARS-CoV-2 in China in late 2019 showed a hyperinflammatory state or cytokine storm, with IL-6 playing a key role in predicting adverse outcomes and mortality. Comorbidities like diabetes and cardiovascular diseases increase the need for anti-cytokine therapy. Recent studies suggest that parthenolide, a natural product from Tanacetum

A retrospective study of 41 COVID-19 patients revealed that while most experienced mild symptoms, some developed aggravated disease and eventually died due to multiple organ dysfunction syndrome caused by a severe cytokine storm. The January 2020 guidelines for treating SARS-CoV-2 pneumonia recommended cytokine monitoring to reduce mortality. The cytokine storm is a significant factor in mortality for various viral diseases, including

A retrospective study of 41 COVID-19 patients revealed that while most experienced mild symptoms, some critically ill patients developed severe cytokine storms leading to multiple organ dysfunction syndrome and death. Guidelines published in late January 2020 recommended cytokine monitoring for severely ill patients to reduce mortality from COVID-19 pneumonia. The cytokine storm is a significant cause of mortality in various viral diseases, including S

Patients with SARS-CoV-2 infections experience immune system changes and inflammatory cytokine storms, leading to multi-organ damage. The NF-kappa-B pathway, which is induced by several mediators, plays a significant role in cytokine storm. Diabetic patients have a higher risk for COVID-19 due to increased virus entry, impaired immunity response, less viral elimination, and dysregulated

A passage titled "Preventing cytokine storm syndrome in COVID-19 using α-1 adrenergic receptor antagonists" suggests that medications that inhibit catecholamine-related inflammation could potentially prevent cytokine storm syndrome in COVID-19 and other diseases.

A retrospective analysis of over 13,000 acute respiratory distress cases and over 108,000 pneumonia cases from various causes found that patients taking alpha-1 adrenergic receptor antagonists (alpha-blockers) had a 35-56% reduced risk of requiring ventilation and dying, compared to non-users. These findings suggest that alpha-blockers may prevent hyperinflammation and ac

The passage discusses the link between severe COVID-19 cases in older adults and those with cardiovascular disorders, attributing their increased risk to progressive atherosclerosis and the role of oxidized LDL (oxLDL) in activating "trained macrophages." These macrophages, when encountering SARS-CoV-2, cause unregulated cytokine secretion and alveolar damage. The hypothesis suggests that pioglit

The passage discusses the higher risk of severe COVID-19 illness in older adults and those with cardiovascular disorders, attributing their increased susceptibility to progressive atherosclerosis and the role of oxidized LDL (oxLDL) in activating "trained macrophages." These macrophages, when encountering SARS-CoV-2, cause unregulated cytokine secretion and alveolar damage. The hypothesis suggests that blocking

Severe COVID-19 shares clinical and laboratory features with hyperferritinemic syndromes, including macrophage activation syndrome, adult-onset Still's disease, catastrophic anti-phospholipid syndrome, and septic shock. Both COVID-19 and hyperferritinemic syndromes are characterized by high serum ferritin and life-threatening hyper-inflammation caused by a cytokine storm leading to

The passage discusses the potential use of Dipeptidyl peptidase-4 (DPP4) inhibitors as a novel therapeutic tool for COVID-19. The virus, SARS-CoV-2, enters cells using both the ACE2 receptor and the DPP4/CD26 receptor. DPP4 is expressed on various epithelia and endothelia, including in the respiratory tract, which may

The severe form of COVID-19 shares similarities with five inflammatory conditions known as "hyperferritinemic syndromes," including macrophage activation syndrome, adult-onset Still's disease, catastrophic anti-phospholipid syndrome, and septic shock. All of these conditions are characterized by high serum ferritin levels and life-threatening hyper-inflammation caused by a cytokine storm that leads

The COVID-19 pandemic caused by SARS-Cov-2 virus has resulted in over 200,000 deaths. Severe patients experience a cytokine storm due to an overactive immune response. Recent reports indicate increased thrombotic events in these patients, which is reflected in the elevated D-dimer levels in hospitalized COVID-19 patients. The connection between the immune system's extreme response and coagulation's extrem

A patient with severe COVID-19 pneumonia experienced rapid worsening but saw improvement after receiving corticosteroids. The background mentions a UK study in June 2020 that found dexamethasone reduced deaths in severe COVID-19 cases. The discussion suggests corticosteroids could benefit patients with an inflammatory profile due to the potential link between severe COVID-19 pneumonia and cytokine storm syndrome. The key take

A worldwide pandemic caused by the new coronavirus SARS-CoV-2 leads to severe acute respiratory syndrome (COVID-19), which can be fatal and is characterized by a cytokine release syndrome (CRS). Efforts are being made to control this "cytokine storm" and save severely affected patients by blocking the signal transduction pathway of pro-inflammatory cytokines. Nicotine, an exogenous

The COVID-19 pandemic is causing a global health crisis, and excessive immune responses leading to cytokine release syndrome (CRS) can be life-threatening. CRS involves the overproduction of pro-inflammatory cytokines such as TNFα, IL-6, and IL-1β. Anecdotal evidence suggests that modulating the immune response could help treat COVID-19 patients. Anti-cytokine therapy, including IL

Severe cases of COVID-19 are causing high mortality rates due to cytokine storms. IL-6 plays a significant role in these storms, and blocking its signal transduction pathway could be an effective treatment. Tocilizumab, an IL-6 receptor blocker, is a promising drug for severe COVID-19 patients as it can effectively block the IL-6 pathway.