scholarly journals Dynamic of Cytokine Storm in Human Inflammatory Response of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-Induced Disease

2021 ◽  
Vol 1808 (1) ◽  
pp. 012054
Author(s):  
A Wiraya ◽  
L Fitriana ◽  
Triyanto ◽  
R Setiawan
2021 ◽  
Vol 22 (15) ◽  
pp. 7914
Author(s):  
So Yeong Cheon ◽  
Bon-Nyeo Koo

The outbreak of the coronavirus disease 2019 (COVID-19) began at the end of 2019. COVID-19 is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and patients with COVID-19 may exhibit poor clinical outcomes. Some patients with severe COVID-19 experience cytokine release syndrome (CRS) or a cytokine storm—elevated levels of hyperactivated immune cells—and circulating pro-inflammatory cytokines, including interleukin (IL)-1β and IL-18. This severe inflammatory response can lead to organ damage/failure and even death. The inflammasome is an intracellular immune complex that is responsible for the secretion of IL-1β and IL-18 in various human diseases. Recently, there has been a growing number of studies revealing a link between the inflammasome and COVID-19. Therefore, this article summarizes the current literature regarding the inflammasome complex and COVID-19.


2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 896.2-896
Author(s):  
M. P. Álvarez ◽  
A. Madrid García ◽  
I. Perez-Sancristobal ◽  
J. I. Colomer ◽  
L. León ◽  
...  

Background:Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), triggers the innate immune system, leading in severe cases, an excessive immune response, which can lead to high levels of pro-inflammatory cytokines promoting a “cytokine storm”.To modulate this exaggerated inflammatory response, several clinical trials with already approved and well-known therapeutic agents that inhibit the inflammatory response, are being carried out. However, none of these drugs seems to achieve the desired results when treating COVID19.Colchicine, a drug often used in the management of patients with Rheumatic and Musculoskeletal diseases (RMDs), is one of the several drugs that are being currently tested for efficacy in COVID19 due to its anti-inflammatory effects.Objectives:To analyze association between colchicine prescription and COVID19-related hospital admissions in patients with Rheumatic and Musculoskeletal diseases (RMDs).Methods:Patients attending a rheumatology outpatient clinic from a tertiary care center in Madrid, Spain, from 1st September 2019 to 29th February 2020 were included.Patients were assigned as exposed or unexposed based on whether they were prescribed with colchicine in their last visit to the clinic during the 6 months before the start of the observation period. Treatment changes during the observation period were also considered. The primary outcome was COVID19-related hospital admissions occurring between March 1st and May 20th, 2020. Secondary outcome included COVID19-related mortality. Several weighting techniques for data balancing, based and non-based on the propensity score, followed by Cox regressions were performed to estimate the association of colchicine prescription on both outcomes.Results:9,379 patients entered in the study, with 406 and 9,002 exposed and unexposed follow-up periods, respectively. Generalized Boosted Models (GBM) and Empirical Balancing Calibration Weighting (EBCW) methods showed the best balance for COVID19-related hospital admissions. Colchicine prescription did not show a statistically significant association after covariable balancing (p-value = 0.195 and 0.059 for GBM and EBCW, respectively). Regarding mortality, the low number of events prevented a success variable balancing and analysis.Conclusion:Colchicine prescription does not play a significant protective or risk role in RMD patients regarding COVID19-related hospital admissions. Our observations could support the maintenance of colchicine prescription in those patients already being treated, as it is not associated with a worse prognosis.References:[1]Fernandez-Gutierrez B. COVID-19 with Pulmonary Involvement. An Autoimmune Disease of Known Cause. Reumatol Clin 2020; 16: 253–254.[2]Coperchini F, Chiovato L, Croce L, et al. The cytokine storm in COVID-19: An overview of the involvement of the chemokine/chemokine-receptor system. Cytokine Growth Factor Rev 2020; 53: 25–32.[3]Shaffer L. 15 drugs being tested to treat COVID-19 and how they would work. Nat Med. Epub ahead of print 15 May 2020. DOI: 10.1038/d41591-020-00019-9.[4]Fernandez-Gutierrez B, Leon L, Madrid A, et al. Hospital admissions in inflammatory rheumatic diseases during the COVID-19 pandemic: incidence and role of disease modifying agents. medRxiv 2020; 2020.05.21.20108696.[5]Freites Nuñez DD, Leon L, Mucientes A, et al. Risk factors for hospital admissions related to COVID-19 in patients with autoimmune inflammatory rheumatic diseases. Ann Rheum Dis 2020; 1–7.Disclosure of Interests:None declared


2021 ◽  
Vol 7 (3) ◽  
pp. 54
Author(s):  
Tobias Plowman ◽  
Dimitris Lagos

The highly infectious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged as the causative agent of coronavirus disease 2019 (COVID-19) in late 2019, igniting an unprecedented pandemic. A mechanistic picture characterising the acute immunopathological disease in severe COVID-19 is developing. Non-coding RNAs (ncRNAs) constitute the transcribed but un-translated portion of the genome and, until recent decades, have been undiscovered or overlooked. A growing body of research continues to demonstrate their interconnected involvement in the immune response to SARS-CoV-2 and COVID-19 development by regulating several of its pathological hallmarks: cytokine storm syndrome, haemostatic alterations, immune cell recruitment, and vascular dysregulation. There is also keen interest in exploring the possibility of host–virus RNA–RNA and RNA–RBP interactions. Here, we discuss and evaluate evidence demonstrating the involvement of short and long ncRNAs in COVID-19 and use this information to propose hypotheses for future mechanistic and clinical studies.


mSphere ◽  
2021 ◽  
Author(s):  
Caiyu Sun ◽  
Mingshan Xue ◽  
Min Yang ◽  
Lihui Zhu ◽  
Yunxue Zhao ◽  
...  

The immune inflammatory response changes rapidly with the progression of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and is responsible for clearance of the virus and further recovery from the infection. However, the intensified immune and inflammatory response in the development of the disease may lead to more serious and fatal consequences, which indicates that immune indicators have the potential to predict serious cases.


2020 ◽  
Author(s):  
Kun Zhao ◽  
Zhang Cao ◽  
Changju Zhu ◽  
Yi Zhang ◽  
Feifan Chen

Abstract Background: SARS-CoV-2 is a newly discovered virus, leading COVID-19 a global threaten nowadays. Case Presentation: The first case of a patient with a thoracic aortic aneurysm (TAA) that became infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported here. The patient died suddenly from a ruptured aorta 19 h after hospital admission. Conclusion: COVID-19 patients with TAA should attract the highest vigilance as COVID-19 might expedite the process of TAA rupture through cytokine storm syndrome, leading to rapid death with little or no warning signs.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Braira Wahid ◽  
Noshaba Rani ◽  
Muhammad Idrees

Abstract After wreaking havoc on a global level with a total of 5,488,825 confirmed cases and 349,095 deaths as of May 2020, severe acute respiratory syndrome coronavirus 2 is truly living up to the expectations of a 21st-century pandemic. Since the major cause of mortality is a respiratory failure from acute respiratory distress syndrome, the only present-day management option is supportive as the transmission relies solely on human-to-human contact. Patients suffering from coronavirus disease 2019 (COVID-19) should be tested for hyper inflammation to screen those for whom immunosuppression can increases chances of survival. As more and more clinical data surfaces, it suggests patients with mild or severe cytokine storms are at greater risk of failing fatally and hence these cytokine storms should be targets for treatment in salvaging COVID-19 patients.


IDCases ◽  
2020 ◽  
pp. e00865
Author(s):  
Shabnam Chettri ◽  
Faryal Khamis ◽  
Nenad Pandak ◽  
Huda Al Khalili ◽  
Elias Said ◽  
...  

IDCases ◽  
2020 ◽  
Vol 21 ◽  
pp. e00829 ◽  
Author(s):  
Shabnam Chhetri ◽  
Faryal Khamis ◽  
Nenad Pandak ◽  
Huda Al Khalili ◽  
Elias Said ◽  
...  

Author(s):  
Afaf Allaoui ◽  
Akif A. Khawaja ◽  
Oussama Badad ◽  
Mariam Naciri ◽  
Marie Lordkipanidzé ◽  
...  

AbstractPlatelets, as nonnucleated blood components, are classically recognized for their pivotal role in hemostasis. In recent years, however, accumulating evidence points to a nonhemostatic role for platelets, as active participants in the inflammatory and immune responses to microbial organisms in infectious diseases. This stems from the ability of activated platelets to secrete a plethora of immunomodulatory cytokines and chemokines, as well as directly interplaying with viral receptors. While much attention has been given to the role of the cytokine storm in the severity of the coronavirus disease 2019 (COVID-19), less is known about the contribution of platelets to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Here, we give a brief overview on the platelet contribution to antiviral immunity and response during SARS-CoV-2 infection.


2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Sema Ketenci ◽  
A. Şükrü Aynacıoğlu

Abstract Background The current coronavirus disease 2019 (COVID-19) outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has emerged in Wuhan, China, and has rapidly become a global challenge, creating major challenges to health systems in almost every country in the world it has turned into a pandemic. COVID-19 poses a risky clinical situation that can range from mild illness to severe respiratory failure, requiring admission to intensive care. Main body It is known that SARS-CoV-2 infection causes a cytokine storm in some critically ill patients. However, more and more evidence showed that there is a dramatic increase in cytokine levels in patients diagnosed with COVID-19. Midkine (MK) is involved in various physiological and pathological processes, which some of them are desired and beneficial such as controlling tissue repair and antimicrobial effects, but some others are harmful such as promoting inflammation, carcinogenesis, and chemoresistance. Also, MK is expressed in inflammatory cells and released by endothelial cells under hypoxic conditions. Conclusions Considering all this information, there are strong data that midkine, an important cytokine known to increase in inflammatory diseases, may be overexpressed in patients who are positive for COVID-19. The overexpression of MK reveals a picture leading to fibrosis and damage in the lung. Therefore, questions arise about how the expression  of  MK  changes in COVID-19 patients and can we use it as an inflammation biomarker or in the treatment protocol in the future.


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