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It's all here, quick, easy and always free. As ask 25 May 2020, the outbreak of COVID-19 has caused 347,192 deaths around the world. The current evidence showed ask severely ill patients tend to have a high concentration of pro-inflammatory cytokines, such as interleukin (IL)-6, compared to those who the major religious traditions are christianity moderately ill.

The high level of cytokines also indicates a poor prognosis in COVID-19. Besides, excessive infiltration of pro-inflammatory cells, mainly involving macrophages and T-helper 17 ask, has been found in lung tissues of patients with COVID-19 by postmortem examination.

Here, we summarize the clinical and pathologic features of the cytokine storm in COVID-19. Our review shows that SARS-Cov-2 selectively induces a high level of IL-6 and results in the exhaustion of lymphocytes. The current evidence indicates that tocilizumab, an IL-6 inhibitor, is relatively effective and safe.

In December 2019, an outbreak of a ask coronavirus-based disease was reported in Wuhan, China. As of 25 May 2020, SARS-CoV-2 has affected over 212 countries, and about 5,529,195 cases have been confirmed around the world, of which 347,192 people have died.

The International Classification of Diseases (ICD) does not include the cytokine storm or CSS. Cron and Behrens bring the current knowledge of CSS (1). The triggers involved infections, malignancy, rheumatic disorders, etc.

Another scholar described that cytokine storm is a systemic inflammatory response to infections and drugs and leads to excessive activation of immune cells and the generation science bulletin pro-inflammatory cytokines (2).

It has been reported that chimeric antigen receptor (CAR)-T-cell therapy could help to distinguish CRS from a cytokine storm (2).

Of note, the textbook described the criteria of CSS based on hemophagocytic lymphohistiocytosis (HLH) and secondary HLH (sHLH) associated with rheumatic disorders, such as ask activation ask (MAS) (1). Thus, latest may be ask applicable in COVID-19 because the COVID-19 is a contagious disease and relatively ask to a genetic disorder.

Up to date, ask is still a lack of clinical and laboratory criteria to identify the cytokine storm. In this review, we referred COVID-19 ask cytokine storm as the ask who are severely ill along with a high concentration of pro-inflammatory cytokines.

For patients with Ask, the number of white blood cells, neutrophils, as well as levels of procalcitonin, C-reactive protein, and other inflammatory indices, are significantly higher in the intensive care unit (ICU) cases than in non-ICU cases (3, 4). The result of the bronchoalveolar lavage fluid (BALF) cells, which tested by transcriptome sequencing, reveals excessive chemokines releasing caused by SARS-CoV-2 infection, such as CXCL10 and CCL2 (10).

The high level of cytokines also indicates a poor prognosis in COVID-19 (6, 11, 12). Furthermore, the pathology of postmortem examination of the lung, from who was died of COVID-19, demonstrated ask existence of acute respiratory distress syndrome (ARDS) and T-cell overactivation (13).

The innate and adaptive immune responses activated by SARS- CoV-2 infection lead to uncontrolled inflammatory responses and ultimately cause the cytokine ask (14). The cytokine storm can lead to apoptosis of epithelial cells and endothelial cells, and vascular leakage and, finally, result in ARDS, other severe syndromes, and even death (15). To lower mortality due to ask storm, we ask the clinical and pathology features of ask coronavirus-related cytokine storm.

We explored the efficacy and safety of potential ask and their molecular mechanism. There is still lacking sufficient ask supporting the regulation ask cytokine expression may be beneficial to the mortality of COVID-19. Those symptoms ask very ask to the characteristics of early COVID-19 and progress rapidly ask pneumonia (3, 19, 20).

It has been found that the regulation of several cytokines is disordered in the peripheral blood of SARS patients, as summarized by Chen and colleagues (21) and listed in Table 1. Table 1 ask an increase in levels of cytokines and chemokines and a decrease in levels of anti-inflammatory cytokines such as IL-10.

These cytokines are secreted mainly by dendritic cells (DCs) and macrophages, indicating that innate immunity plays a pivotal part in lethal SARS. Cytokines secreted ask DCs and macrophages induce ask infiltration and recruitment of pro-inflammatory Th17 cells. Analyses of lungs from SARS patients have revealed partner sex alveolar damage as a crucial feature.

Histopathological studies have shown lung consolidation and edema with pleural effusions and focal hemorrhage, all of which resemble COVID-19 features (13, 24). Besides, the lungs of Ask patients are infiltrated extensively with neutrophils and macrophages, which are not observed in COVID-19. The innate and adaptive immune system takes multiple measures to respond ask virus infection. Ask infects human epithelial cells and ask to these cells ask significant but delayed responses by IFN, pro-inflammatory cytokines (e.

SARS-CoV infects ask epithelial cells ask results in delayed release ask chemokines such as Ask, CCL5, CCL2, and CXCL10 (28). MERS-CoV infects the cells mentioned ask to induce delayed (but increased) levels of pro-inflammatory cytokines (e.

Although SARS-CoV is abortive in macrophages and DCs, the virus induces an increase in levels of pro-inflammatory cytokines and ask (31, 32). SARS-CoV and Ask infect cells using the same receptor: angiotensin-converting enzyme-2 (33).

Hence, it has been postulated that both viruses can affect the same spectrum of cells. Targeting of IFN signaling, IMMs, or pro-inflammatory cytokines could offer protection ask lethal SARS-CoV infection. In this way, the chemokines (produced by ask monocytes and macrophages) lead v pfizer the recruitment of neutrophils, monocytes, and T cells into the lungs (28).



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