scholarly journals COVID-19 and Cytokine Storm

2020 ◽  
Author(s):  
Mustafa Kurtuluş ◽  
İbrahim Pirim
Keyword(s):  
Immune Response ◽  
Host Response ◽  
Distress Syndrome ◽  
Multiple Organ ◽  
Past Century ◽  
Viral Agent ◽  
Disease Course ◽  
Cytokine Storm ◽  
The Past ◽  
Novel Coronavirus

Although the etiopathogenesis of infections has been largely illuminated by technical and scientific developments in the past century; many issues are still not clear today. The word “there is no disease, there is a patient” is stil valid today. Because the immune response of the host is as important as the virulence of the pathogen in infections and disease course can vary a lot according to the person. Cytokine Storm is seen exactly in a group of diseases where the host response is very prominent. For this reason, Cytokine Storm Syndrome (CSS) is mostly mentioned. CSS emerging due to different inflammatory etiologies; it is an overwhelming systemic inflammation, hemodynamic imbalance, multiple organ failure, and potentially leading to death. After being first seen in Influenza in 2003 as a viral agent, CSS was seen in SARS-Cov, MERS-CoV and SARS-CoV2, which were found to be the las thuman disease from the Corona viridea family.The novel coronavirus SARS-CoV2 causes COVID-19, a pandemic threatening millions. Uncontrolled production of pro-inflammatory mediators contributes to, acut respiratory distress syndrome (ARDS) and cytokine storm syndrome in COVID-19.

scholarly journals Estradiol, Progesterone, Immunomodulation, and COVID-19 Outcomes

Endocrinology ◽  
2020 ◽  
Vol 161 (9) ◽  
Author(s):  
Franck Mauvais-Jarvis ◽  
Sabra L Klein ◽  
Ellis R Levin
Keyword(s):  
Immune Response ◽  
Distress Syndrome ◽  
Immune Dysregulation ◽  
Innate Immune ◽  
The Novel ◽  
Cytokine Storm ◽  
Inflammatory Infiltration ◽  
Biological Sex ◽  
17Β Estradiol ◽  
Novel Coronavirus

Abstract Severe outcomes and death from the novel coronavirus disease 2019 (COVID-19) appear to be characterized by an exaggerated immune response with hypercytokinemia leading to inflammatory infiltration of the lungs and acute respiratory distress syndrome. Risk of severe COVID-19 outcomes is consistently lower in women than men worldwide, suggesting that female biological sex is instrumental in protection. This mini-review discusses the immunomodulatory and anti-inflammatory actions of high physiological concentrations of the steroids 17β-estradiol (E2) and progesterone (P4). We review how E2 and P4 favor a state of decreased innate immune inflammatory response while enhancing immune tolerance and antibody production. We discuss how the combination of E2 and P4 may improve the immune dysregulation that leads to the COVID-19 cytokine storm. It is intended to stimulate novel consideration of the biological forces that are protective in women compared to men, and to therapeutically harness these factors to mitigate COVID-19 morbidity and mortality.

scholarly journals Vitamin D regulation of the immune system and its implications for COVID-19: A mini review

2021 ◽  
Vol 9 ◽  
pp. 205031212110140
Author(s):  
Linda Bui ◽  
Zahra Zhu ◽  
Stephanie Hawkins ◽  
Alonso Cortez-Resendiz ◽  
Alfredo Bellon
Keyword(s):  
Vitamin D ◽  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Symptoms ◽  
Distress Syndrome ◽  
Clinical Presentation ◽  
Potential Contribution ◽  
The Novel ◽  
Cytokine Storm ◽  
Novel Coronavirus

The novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is at the origin of the current pandemic, predominantly manifests with severe respiratory symptoms and a heightened immune response. One characteristic of SARS-CoV-2 is its capacity to induce cytokine storm leading to acute respiratory distress syndrome. Consequently, agents with the ability to regulate the immune response, such as vitamin D, could become tools either for the prevention or the attenuation of the most severe consequences of the coronavirus disease 2019 (COVID-19). Vitamin D has shown antimicrobial as well as anti-inflammatory properties. While SARS-CoV-2 promotes the release of proinflammatory cytokines, vitamin D attenuates the release of at least some of these same molecules. Inflammatory cytokines have been associated with the clinical phenomena of COVID-19 and in particular with its most dangerous complications. Therefore, the goals of this article are as follows: first, present the numerous roles vitamin D plays in modulating the immune response; second, gather data currently available on COVID-19 clinical presentation and its relation to cytokines and similar molecules; third, expose what it is known about how coronaviruses elicit an inflammatory reaction; and fourth, discuss the potential contribution of vitamin D in reducing the risk and severity of COVID-19.

scholarly journals The use of mesenchymal stromal cells in the treatment of coronavirus disease 2019

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Maurice A. Canham ◽  
John D. M. Campbell ◽  
Joanne C. Mountford
Keyword(s):  
Multiple Sclerosis ◽  
Clinical Trial ◽  
Immune Response ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Host Response ◽  
Distress Syndrome ◽  
Graft Versus Host ◽  
Immunomodulatory Properties ◽  
Efficacious Vaccine

Abstract More than seven months into the coronavirus disease -19 (COVID-19) pandemic, infection from the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has led to over 21.2 million cases and resulted in over 760,000 deaths worldwide so far. As a result, COVID-19 has changed all our lives as we battle to curtail the spread of the infection in the absence of specific therapies against coronaviruses and in anticipation of a proven safe and efficacious vaccine. Common with previous outbreaks of coronavirus infections, SARS and Middle East respiratory syndrome, COVID-19 can lead to acute respiratory distress syndrome (ARDS) that arises due to an imbalanced immune response. While several repurposed antiviral and host-response drugs are under examination as potential treatments, other novel therapeutics are also being explored to alleviate the effects on critically ill patients. The use of mesenchymal stromal cells (MSCs) for COVID-19 has become an attractive avenue down which almost 70 different clinical trial teams have ventured. Successfully trialled for the treatment of other conditions such as multiple sclerosis, osteoarthritis and graft versus host disease, MSCs possess both regenerative and immunomodulatory properties, the latter of which can be harnessed to reduce the severity and longevity of ARDS in patients under intensive care due to SARS-CoV-2 infection.

scholarly journals How to Control Covid-19 with a Nanobiotherapy?

2020 ◽  
Keyword(s):  
Intensive Care Unit ◽  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Multiple Organ ◽  
World Health ◽  
Shortness Of Breath ◽  
The World ◽  
Health Organization ◽  
Muscle Ache

The outbreak of emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease (COVID-19) in China has been brought to global attention and declared a pandemic by the World Health Organization (WHO) on March 11, 2020. In a recent study of Nanshan Chen et al., on patients of Wuhan Jinyintan Hospital, Wuhan, China, from the 99 patients with SARSCoV-2 infection, 51% had chronic diseases and they had symptoms of fever (83%), cough (82%) shortness of breath (31%), muscle ache (11%), fatigue (9%), headache (8%), sore throat (5%), rhinorrhea (4%), chest pain (2%), diarrhea (2%), and nausea and vomiting (1%) [1, 2]. The majority of patients can recover, however, about 25% of patients will progress into severe complications including acute respiratory distress syndrome (ARDS), which may worsen rapidly into respiratory failure, need an intensive care unit (ICU) and even cause multiple organ failure [3]. Depending on the pathophysiological mechanisms supposed to be involved in the development of the various clinical forms of the disease, various types of treatment have been tested with varying degrees of success. We have developed a nanotherapy to block the entry of the virus into the host cell, to reduce its potential for replication and to regulate the immune response against the microbial aggressor [4].

scholarly journals POTENTIAL THERAPIES FOR TREATMENT OF COVID-19

2020 ◽  
Vol 7 (1) ◽  
pp. 062-071
Author(s):  
Beatriz Gasser ◽  
Ricardo Andres Ramirez Uscategui
Keyword(s):  
Clinical Trials ◽  
Distress Syndrome ◽  
Multiple Organ ◽  
The Novel ◽  
Controlled Clinical Trials ◽  
Interferon Β ◽  
The World ◽  
Novel Coronavirus ◽  
Time Point

Since discovery of the novel coronavirus (SARS-CoV-2) in December of 2019, this viral pneumonia originated in Wuhan, China quickly spread around the world. This new disease, called COVID-19 can cause Acute Respiratory Distress Syndrome (ARDS) due to an uncontrolled inflammatory response like sepsis, that leads to multiple organ failure and even death. Several pharmacotherapeutics alternatives are being tested over the world, looking for most diverse drugs that might be able to fight the infection. The objective of this paper is to review the main pharmacotherapeutics techniques development, as remdesivir, chloroquine/hydroxychloroquine, lopinavir plus ritonavir, interferon-β, ivermectin, anticoagulants, convalescent plasma and vaccine, currently undergoing clinical trials in order to evaluate its effectiveness and safety to combat the COVID-19, presenting their characteristics, possible adverse effects and main scientific findings of its potential action. In conclusion, some therapies presented promising in-vitro results or in the treatment of some patients, nonetheless, multicentric blinded placebo controlled clinical trials are necessary to determine their effectiveness, safety, dosage, and best time point of treatment.

scholarly journals Early Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus Infection

2009 ◽  
Vol 83 (14) ◽  
pp. 7062-7074 ◽  
Author(s):  
Barry Rockx ◽  
Tracey Baas ◽  
Gregory A. Zornetzer ◽  
Bart Haagmans ◽  
Timothy Sheahan ◽  
...  
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Severe Acute Respiratory Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Host Response ◽  
Molecular Mechanisms ◽  
Distress Syndrome ◽  
Aged Mice ◽  
Young Mice

ABSTRACT Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.

scholarly journals The Use of Dupilumab in Atopic Dermatitis During Coronavirus Disease-19 Era – A Review

2020 ◽  
Vol 8 (T1) ◽  
pp. 399-407
Author(s):  
Laura Pauline Kosasih
Keyword(s):  
Atopic Dermatitis ◽  
Distress Syndrome ◽  
Multiple Organ ◽  
Cytokine Storm ◽  
T Helper ◽  
Immunomodulatory Treatment ◽  
Global Pandemic ◽  
Common Causes ◽  
Th 1 ◽  
Vast Range

The global pandemic of coronavirus (CoV) d0isease 2019 (COVID-19), caused by severe acute respiratory syndrome CoV (SARS-CoV 2), has been a challenging event for every individual. It is known that COVID-19 may exhibit a vast range of symptoms ranging from mild to severe. Acute respiratory distress syndrome (ARDS) and multiple organ failure are the most common causes of death in COVID-19 cases [3]. Accumulating evidence shows that T-helper type (Th-1) inflammation cascade plays a major role in COVID-19 pathogenesis. It is proposed that aberrant immune reaction, or known as cytokine storm, is one of the main causals of ARDS in COVID-19 case, while dupilumab, the first Food and Drug Administration-approved immunomodulatory treatment for atopic dermatitis, is known for its effectiveness in suppressing the Th-2 inflammation pathway. It is postulated that both types of inflammation can cross-regulate each other. Therefore, some may believe that the regression of Th-2 cascade may upregulate the Th-1 cascade, leading to an exaggerated cytokine storm. This hypothesis leads to the uncertainty of the safety of continuing this modality during the pandemic.

scholarly journals Immune Response to COVID-19

2021 ◽  
Author(s):  
Ricardo Wesley Alberca
Keyword(s):  
Immune Response ◽  
Adaptive Immune Response ◽  
Multiple Organ ◽  
Disease Course ◽  
Angiotensin Converting Enzyme 2 ◽  
Damage And Failure ◽  
Adaptive Immune ◽  
General Aspects ◽  
Inflammatory Molecules ◽  
The Impact

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) invades the host’s cells via the angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). ACE2 and TMPRSS2 molecules are highly expressed on the respiratory tract but are also expressed in other organs such as kidneys, heart, and intestine, which could partially explain the multiple organ infection, damage, and failure. During the COVID-19 disease course, patients may develop a dysregulation in the immune response, with an exacerbated production of pro-inflammatory molecules and hypercoagulation, which can collaborate to the increase in tissue damage and death. This chapter will cover general aspects of the innate and adaptive immune response during COVID-19, the impact of comorbidities on the immune response to SARS-CoV-2, and the immune response generated by COVID-19 vaccines.

scholarly journals Covid-19 and leptospirosis: Cytokine storm and the use of steroids

2020 ◽  
pp. 004947552097142
Author(s):  
Abraham M Ittyachen
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Distress Syndrome ◽  
Multiple Organ ◽  
The Other ◽  
High Dose ◽  
Cytokine Storm ◽  
The World ◽  
The Common ◽  
Precipitating Factor

The majority of patients with Covid-19 have a good outcome. However, complications principally of acute respiratory distress syndrome (ARDS) and multiple-organ failure can occur rapidly. Leptospirosis, a zoonotic disease, is similar to Covid-19 in that most infections are mild or asymptomatic and only a small number develop ARDS. Cytokine storm is considered to be the main incriminating factor in both. High dose steroids have been used to ameliorate the effects in leptospirosis, and similarly, reports suggest a benefit in Covid-19. SARS CoV-2 and leptospira, one a virus and the other a bacterium, are two species separated by millions of years of evolution, but producing illnesses with similar spectra, with cytokine storm being the common precipitating factor. As data are accrued from around the world, more light may be shed on features analogous to both pathways.

scholarly journals COVID-19. A review

2020 ◽  
Vol 90 (2) ◽  
Author(s):  
Irappa Madabhavi ◽  
Malay Sarkar ◽  
Nagaveni Kadakol
Keyword(s):  
Distress Syndrome ◽  
Case Fatality ◽  
Genomic Analysis ◽  
Multiple Organ ◽  
Low Grade ◽  
Epidemic Outbreak ◽  
Wuhan City ◽  
Novel Coronavirus ◽  
The Universe ◽  
Highly Virulent

The enduring epidemic outbreak which started in Wuhan city of China, in December 2019 caused by the 2019 novel coronavirus (COVID- 19) or the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has created a dangerous and deadly Public Health disaster of International apprehension, with cases confirmed in several countries. This novel community health trouble is frightening the universe with clinical, psychological, emotional, collapse of health system and economical slowdown in each and every part of the world infecting nearly 200 countries. A highly virulent and pathogenic COVID-19 viral infection with incubation period ranging from two to fourteen days, transmitted by breathing of infected droplets or contact with infected droplets, belongs to the genus Coronavirus with its high mutation rate in the Coronaviridae. The likely probable primary reservoir could be bats, because genomic analysis discovered that SARSCoV-2 is phylogenetically interrelated to SARS-like bat viruses. The transitional resource of origin and transfer to humans is not known, however, the rapidly developing pandemic has confirmed human to human transfer. Approximately 1,016,128 reported cases, 211,615 recovered cases and 53,069 deaths of COVID-2019 have been reported to date (April 2, 2020). The symptoms vary from asymptomatic, low grade pyrexia, dry cough, sore throat, breathlessness, tiredness, body aches, fatigue, myalgia, nausea, vomiting, diarrhea, to severe consolidation and pneumonia, acute respiratory distress syndrome (ARDS) and multiple organ dysfunction leading to death with case fatality rate ranging from 2 to 3%.

Sign in / Sign up

Export Citation Format

Share Document