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 SARS CoV-2 Might Exploit Cells of the Innate Immune System to Induce the Novel Acute Immune Dysrhythmic Syndrome (n-AIDS) and Para COVID-19 Syndrome.

2021 ◽  
Author(s):  
Mina Kelleni
Keyword(s):  
Immune Response ◽  
Innate Immune System ◽  
Langerhans Cells ◽  
Interesting Case ◽  
Innate Immune ◽  
Delayed Type Hypersensitivity ◽  
The Novel ◽  
Cytokine Storm ◽  
Humoral Immune ◽  
Cytokines And Chemokines

In this manuscript, we combine our insights towards COVID-19 to present a hypothesis that might explain its pathogenesis and complications while presenting an interesting case report of post COVID-19 allergic cell mediated (dysregulated) delayed type hypersensitivity. Moreover, we confirm our call to reclassify it as novel acute immune dysrhythmic syndrome (n-AIDS) to include both cytokine storm and we suggest to describe post or long COVID and other autoimmune complications as para COVID-19 syndrome. We suggest that SARS CoV-2 might exploit monocytes, macrophages and tissue resident macrophages including skin Langerhans cells to induce dysregulated cellular and humoral immune response through known and yet to be discovered cytokines and chemokines to ultimately induce the cytokine storm and/or autoimmune responses.

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 SARS-CoV-2 infection and the antiviral innate immune response

2020 ◽  
Author(s):  
Hui Yang ◽  
Yingying Lyu ◽  
Fajian Hou
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Clinical Manifestations ◽  
Innate Immune ◽  
World Health ◽  
The Novel ◽  
Global Public Health ◽  
Replication Process ◽  
Novel Coronavirus ◽  
Health Organization

Abstract The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak began in December 2019, causing the illness known as the novel coronavirus disease 2019 (COVID-19). The virus spread rapidly worldwide to become a global public health emergency. As of 15 November 2020, more than 53 million confirmed cases and over one million deaths worldwide have been reported (World Health Organization, 2020). The SARS-CoV-2 genome was sequenced and studies are ongoing to further understand the epidemiology, clinical manifestations, etiological structure, cellular receptor angiotensin II converting enzyme (ACE2), and intracellular replication process of the virus. Currently, thousands of clinical trials related to SARS-CoV-2 are underway (https://clinicaltrials.gov/). However, no vaccines or drugs have yet been approved, until very recently, for direct treatment or prevention of COVID-19 and only supportive treatment has been applied clinically. This review will discuss the possible mechanism of the innate immune response to SARS-CoV-2 infection and provide insight into the development of related therapeutics.

scholarly journals Cytokine Storm: The Primary Determinant for the Pathophysiological Evolution of COVID-19 Deterioration

2021 ◽  
Vol 12 ◽  
Author(s):  
Ruirong Chen ◽  
Zhien Lan ◽  
Jujian Ye ◽  
Limin Pang ◽  
Yi Liu ◽  
...  
Keyword(s):  
Immune Response ◽  
Acute Respiratory Distress Syndrome ◽  
Immune System ◽  
Severe Acute Respiratory Syndrome ◽  
Distress Syndrome ◽  
The Novel ◽  
Cytokine Storm ◽  
Major Threat ◽  
Primary Determinant ◽  
Multi Organ Dysfunction Syndrome

The coronavirus disease 2019 (COVID-19) pandemic caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an ongoing major threat to global health and has posed significant challenges for the treatment of severely ill COVID-19 patients. Several studies have reported that cytokine storms are an important cause of disease deterioration and death in COVID-19 patients. Consequently, it is important to understand the specific pathophysiological processes underlying how cytokine storms promote the deterioration of COVID-19. Here, we outline the pathophysiological processes through which cytokine storms contribute to the deterioration of SARS-CoV-2 infection and describe the interaction between SARS-CoV-2 and the immune system, as well as the pathophysiology of immune response dysfunction that leads to acute respiratory distress syndrome (ARDS), multi-organ dysfunction syndrome (MODS), and coagulation impairment. Treatments based on inhibiting cytokine storm-induced deterioration and occurrence are also described.

scholarly journals Interplay of Opposing Effects of the WNT/β-Catenin Pathway and PPARγ and Implications for SARS-CoV2 Treatment

2021 ◽  
Vol 12 ◽  
Author(s):  
Alexandre Vallée ◽  
Yves Lecarpentier ◽  
Jean-Noël Vallée
Keyword(s):  
Distress Syndrome ◽  
The Novel ◽  
Cytokine Storm ◽  
Angiotensin Converting Enzyme 2 ◽  
Tnf Α ◽  
Pparγ Agonists ◽  
Novel Coronavirus ◽  
Opposing Effects ◽  
Canonical Wnt

The Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), has quickly reached pandemic proportions. Cytokine profiles observed in COVID-19 patients have revealed increased levels of IL-1β, IL-2, IL-6, and TNF-α and increased NF-κB pathway activity. Recent evidence has shown that the upregulation of the WNT/β-catenin pathway is associated with inflammation, resulting in a cytokine storm in ARDS (acute respire distress syndrome) and especially in COVID-19 patients. Several studies have shown that the WNT/β-catenin pathway interacts with PPARγ in an opposing interplay in numerous diseases. Furthermore, recent studies have highlighted the interesting role of PPARγ agonists as modulators of inflammatory and immunomodulatory drugs through the targeting of the cytokine storm in COVID-19 patients. SARS-CoV2 infection presents a decrease in the angiotensin-converting enzyme 2 (ACE2) associated with the upregulation of the WNT/β-catenin pathway. SARS-Cov2 may invade human organs besides the lungs through the expression of ACE2. Evidence has highlighted the fact that PPARγ agonists can increase ACE2 expression, suggesting a possible role for PPARγ agonists in the treatment of COVID-19. This review therefore focuses on the opposing interplay between the canonical WNT/β-catenin pathway and PPARγ in SARS-CoV2 infection and the potential beneficial role of PPARγ agonists in this context.

scholarly journals Cytokine Storms, Evolution, and COVID-19

2021 ◽  
Author(s):  
Joe Alcock ◽  
Alix Masters
Keyword(s):  
Immune Response ◽  
Evolutionary Medicine ◽  
Severe Illness ◽  
Host Immune System ◽  
The Novel ◽  
Cytokine Storm ◽  
Medical Interventions ◽  
Experimental Therapies ◽  
Novel Coronavirus

Abstract Since the identification of severe illness caused by the novel coronavirus SARS-CoV-2, the role of the host immune system in causing disease has attracted widespread attention, along with intense interest in medical interventions that target the host immune response. A wide variety of agents have been proposed to treat a cytokine storm in COVID-19, but so far, only one class of medications, corticosteroids, has proved useful. In recent decades, experimental therapies for cytokine storms have been tried and mostly failed to help patients with severe sepsis and other infections. We summarize this history in order to frame expectations for novel interventions in COVID-19 and to bring an evolutionary medicine perspective to the concept of cytokine storms and their treatment.

scholarly journals Alpha-1 antitrypsin inhibits TMPRSS2 protease activity and SARS-CoV-2 infection

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lukas Wettstein ◽  
Tatjana Weil ◽  
Carina Conzelmann ◽  
Janis A. Müller ◽  
Rüdiger Groß ◽  
...  
Keyword(s):  
Serine Protease ◽  
Immune Defense ◽  
Innate Immune ◽  
Respiratory Pathogen ◽  
The Novel ◽  
Airway Epithelial ◽  
Protein Library ◽  
Epithelial Cultures ◽  
Alpha 1 Antitrypsin ◽  
Novel Coronavirus

AbstractSARS-CoV-2 is a respiratory pathogen and primarily infects the airway epithelium. As our knowledge about innate immune factors of the respiratory tract against SARS-CoV-2 is limited, we generated and screened a peptide/protein library derived from bronchoalveolar lavage for inhibitors of SARS-CoV-2 spike-driven entry. Analysis of antiviral fractions revealed the presence of α1-antitrypsin (α1AT), a highly abundant circulating serine protease inhibitor. Here, we report that α1AT inhibits SARS-CoV-2 entry at physiological concentrations and suppresses viral replication in cell lines and primary cells including human airway epithelial cultures. We further demonstrate that α1AT binds and inactivates the serine protease TMPRSS2, which enzymatically primes the SARS-CoV-2 spike protein for membrane fusion. Thus, the acute phase protein α1AT is an inhibitor of TMPRSS2 and SARS-CoV-2 entry, and may play an important role in the innate immune defense against the novel coronavirus. Our findings suggest that repurposing of α1AT-containing drugs has prospects for the therapy of COVID-19.

scholarly journals Still’s Disease in the Constellation of Hyperinflammatory Syndromes: A Link with Kawasaki Disease?

2021 ◽  
Vol 10 (15) ◽  
pp. 3244
Author(s):  
Perrine Dusser ◽  
Isabelle Koné-Paut
Keyword(s):  
Immune Response ◽  
Kawasaki Disease ◽  
Innate Immune Response ◽  
Adaptive Response ◽  
Genetic Factors ◽  
Innate Immune ◽  
Cytokine Storm ◽  
Still’S Disease ◽  
Still's Disease ◽  
Excessive Activation

Still’s disease and Kawasaki disease (KD) today belong to the group of cytokine storm syndromes, a pathophysiological set related to excessive activation of the innate immune response. We present here a personal vision of what can link these two diseases, taking up their concepts at their beginning. By their many clinical and physiopathological similarities, we conclude that they constitute a common spectrum whose fate is modified by subtle differences in terms of adaptive response that could, in part, be driven by genetic factors.

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