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In the beginning of the third year of the fight against COVID-19, the virus remains at least still one step ahead in the pandemic "war". The key reasons are evolving lineages and mutations, resulting in an increase of transmissibility and ability to evade immune system. However, from the immunologic point of view, the cytokine storm (CS) remains a poorly understood and difficult to combat culprit of the extended number of in-hospital admissions and deaths. It is not fully clear whether the cytokine release is a harmful result of suppression of the immune system or a positive reaction necessary to clear the virus. To develop methods of appropriate treatment and therefore decrease the mortality of the so-called COVID-19-CS, we need to look deeply inside its pathogenesis, which is the purpose of this review. [ABSTRACT FROM AUTHOR]

In March 2020, COVID-19 infection caused by SARS-CoV-2 has been declared to be a global pandemic, where its complications, severity and mortality are reported to be due to the released inflammatory cytokines or the so-called cytokine storm. This is quite similar to that observed in the autoimmune and chronic inflammatory rheumatic disease, rheumatoid arthritis (RA). It was hypothesized that RA patients are at a higher risk of acquiring COVID-19; however, recent studies reported that they are not when compared to the rest of the population. In this review, we aim to highlight the mutual pathological features, cytokine profiles and risk factors between COVID-19 and RA. Also, many researchers are currently working to explore therapeutic agents that could aid in the eradication of COVID-19 infection. Due to the similarity between the inflammation status in COVID-19 and RA, many anti-rheumatic drugs such as hydroxychloroquine, tocilizumab, baricitinib and anakinra were proposed to be therapeutic modalities for COVID-19 infection. [ABSTRACT FROM AUTHOR]

• The "cytokine storm" is one of the most dangerous and potentially life-threatening event related to COVID-19 sustaining its major clinical complications. • Early studies already indicated that the chemokine/chemokine receptor system largely contributed to the onset of the "cytokine storm". • Rapidly growing evidences supported a major role of specific chemokines in driving a more or less severe clinical course of Sars-Cov-2 infection. • At the present, CXCL10 and CCL2 represent, at the present, the chemokines identified to play a major role in driving a more severe course of COVID-19, potentially serving as a marker for predicting the clinical outcome. • Owing to the great effort of the Scientific Community, in increasing our knowledge on COVID-19, it is likely that also other chemokines will be further investigated in the next future. SARS-COV-2 infection represents the greatest pandemic of the world, counting daily increasing number of subjects positive to the virus and, sadly, increasing number of deaths. Current studies reported that the cytokine/chemokine network is crucial in the onset and maintenance of the "cytokine storm", the event occurring in those patients in whom the progression of COVID-19 will progress, in most cases, to a very severe and potentially threatening disease. Detecting a possible "immune signature" in patients, as assessed by chemokines status in patients with COVID-19, could be helpful for individual risk stratification for developing a more or less severe clinical course of the disease. The present review is specifically aimed at overviewing current evidences provided by in vitro and in vivo studies addressing the issue of which chemokines seems to be involved, at least at present, in COVID-19. Currently available experimental and clinical studies regarding those chemokines more deeply studied in COVID-19, with a specific focus on their role in the cytokine storm and ultimately with their ability to predict the clinical course of the disease, will be taken into account. Moreover, similarities and differences between chemokines and cytokines, which both contribute to the onset of the pro-inflammatory loop characterizing SARS-COV-2 infection, will be briefly discussed. Future studies will rapidly accumulate in the next months and their results will hopefully provide more insights as to the complex physiopathology of COVID-19-related cytokine storm. This will likely make the present review somehow "dated" in a short time, but still the present review provides an overview of the scenario of the current knowledge on this topic. [ABSTRACT FROM AUTHOR]

Rapidly spreading outbreak of the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is causing serious health concerns worldwide. It started as an epidemic in Wuhan, Hubei province, central China, and has now become a pandemic, spreading over most of the continents of the planet. The major clinical symptoms of the infection are dry cough, fever, pneumonia, respiratory failure, hypoxia, and in certain cases, even death. Alveolar damage and respiratory system failure are observed in severe cases. Initial mild infection leads to activation of the immune system in the lungs and accumulation of various inflammatory cells and molecules. At a later phase during the infection, a "cytokine storm" causes an Acute Respiratory Distress Syndrome (ARDS), leading to an increase in the production of pro-inflammatory cytokines, migration of a large number of immune cells to the site of infection, and ultimately pulmonary damage. The rapid and uncontrolled outbreak requires putative therapeutic drugs for treatment of patients suffering from COVID-19. Amongst the currently used antiviral drugs, such as hydroxychloroquine, lopinavir, remdesivir etc. we would like to present an update on another effective drug, pentoxifylline. Pentoxifylline has anti-inflammatory, immunomodulatory, anti-viral, and bronchodilatory properties. Pentoxifylline is known to reduce cytokine production, immune cell migration, and suppress certain signal transduction pathways (e.g. NF-ĸβ and STAT3). Thus, it minimizes inflammatory damage in the lung tissues. [ABSTRACT FROM AUTHOR]

Rapidly spreading outbreak of the novel Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is causing serious health concerns worldwide. It started as an epidemic in Wuhan, Hubei province, central China, and has now become a pandemic, spreading over most of the continents of the planet. The major clinical symptoms of the infection are dry cough, fever, pneumonia, respiratory failure, hypoxia, and in certain cases, even death. Alveolar damage and respiratory system failure are observed in severe cases. Initial mild infection leads to activation of the immune system in the lungs and accumulation of various inflammatory cells and molecules. At a later phase during the infection, a “cytokine storm” causes an Acute Respiratory Distress Syndrome (ARDS), leading to an increase in the production of pro-inflammatory cytokines, migration of a large number of immune cells to the site of infection, and ultimately pulmonary damage. The rapid and uncontrolled outbreak requires putative therapeutic drugs for treatment of patients suffering from COVID-19. Amongst the currently used antiviral drugs, such as hydroxychloroquine, lopinavir, remdesivir etc. we would like to present an update on another effective drug, pentoxifylline. Pentoxifylline has anti-inflammatory, immunomodulatory, anti-viral, and bronchodilatory properties. Pentoxifylline is known to reduce cytokine production, immune cell migration, and suppress certain signal transduction pathways (e.g. NF-κβ and STAT3). Thus, it minimizes inflammatory damage in the lung tissues. [ABSTRACT FROM AUTHOR]