Introduction: The virus's cytopathic effects and ability to evade the host defense system are thought to play a role in the severity of COVID-19 disease .The host immune system can lead to a fatal inflammatory condition known as CRS in COVID-19 individuals. This is a phenomenon of an excessive inflammatory response, as the name implies, in which inflammatory cytokines are swiftly and massively released in response to infective stimuli. This uncontrolled inflammatory cytokine storm is a serious condition that is seen in patients who need to be admitted to the intensive care unit (ICU). This study sought to determine whether there was any connection between cytokine storm and the underlying causes of corona illness with its severe symptoms.
Methods: This study was conducted to Relationship between cytokine storm and the
causes of corona disease with severe symptoms based on scientific databases such as
Science Direct, Springer, Google Scholar, and PubMed.
Results: The findings indicated that CRS is one of the potential triggers for the fatal and progressive types of COVID-19. Clinical criteria for CRS are difficult to define, however current research suggests several characteristics, including clinical symptoms and test results, to support this status. Although there are many theories, it is still unclear what causes inflammatory substances to be released without restriction. The first is a result of viral replication, which triggers pyroptosis, a particularly inflammatory type of lytic-programmed cell death (apoptosis). Pyroptosis disrupts macrophage and lymphocyte activities, releases pro-inflammatory cytokines, and results in peripheral lymphopenia in COVID-19 patients. Interferon (INF)-1 may modify innate immunity, according to mounting evidence. INF-1 has a critical role in supporting adaptive immune systems and viral proliferation. It is true that COVID-19 affects the host's innate immune response and reduces INF-1's ability to operate in response to infection. As the body's initial line of defense after a virus infection, macrophages, dendritic cells, and neutrophils initiate the immunological response. Moreover, recent studies suggest that excessive production of some cytokines, such as IL-6, may be the primary cause of the inflammatory response in COVID-19. The second hypothesis is related to adaptive immunity and the production of neutralizing antibodies against the surface antigen of the virus. Lung autopsies from patients who died from COVID-19 showed a high infiltration of macrophages into the bronchial mucosa. Immunoglobulin (Ig) Gs were reported to attach to the S protein and initiate inflammatory cascades in some animal investigations. Through the production of IL-8 and monocyte chemoattractant protein (MCP)-1, this binding can increase the number of pro-inflammatory macrophages and monocytes in the lungs. The virus anti-S-IgG complex interacts with the Fc receptor (FcR) on the surface of monocytes and macrophages to cause an inflammatory response. The fact that pro-inflammatory cytokine levels dropped when macrophage receptors were blocked lends credence to this idea. Additionally, many pieces of evidence show that the development of severe respiratory disease in COVID-19 patients coincides with the presence of anti-viral IgGs.
Conclusion: Conclusion and views the cytokine storm in COVID-19 may be caused by dysregulated acquired immune system and hyperinflammatory innate immune responses. In this article, we first examined putative pathways underlying the COVID-19-induced CRS before outlining potential treatment options. In fact, in critically ill COVID-19 patients, the CRS is directly related to catastrophic outcomes. The survival rate of infected patients may increase with the use of immunomodulatory drugs and cytokine antagonists to control the cytokine storm. The therapeutic efficacy of antiviral medication in COVID-19 patients can be improved by focusing on inflammatory cytokines in this regard. On the other hand, because the inflammatory network is so complicated, focusing on a single inflammatory signaling pathway can trigger later compensatory immune responses. Therefore, it is important to weigh the advantages and disadvantages of using anti-inflammatory medications. According to the data presented here and the authors' point of view, inflammatory cytokine-targeting antibodies continue to be a popular therapeutic strategy. As a result, combination therapy using inflammatory inhibitors and other COVID-19 modalities may be more effective than either strategy used alone. To comprehend the fundamental mechanism of cytokine storms in COVID-19, highly credible evidence is needed. To clarify the significance of anti-inflammatory therapies to control excessive inflammation, more research is required.