SARS-CoV-2 and helminth co-infections, and environmental pollution exposure: An epidemiological and immunological perspective
Pragalathan NaidooTerisha GhaziAnil A. ChuturgoonRajen N. NaidooVeron RamsuranMiranda N. Mpaka-MbathaKhethiwe N. BhenguNomzamo NembeZamathombeni DumaRoxanne PillayRavesh SinghZilungile L. Mkhize‐Kwitshana
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Soil-transmitted helminths infect billions of people globally, particularly those residing in low- and middle-income regions with poor environmental sanitation and high levels of air and water pollution. Helminths display potent immunomodulatory activity by activating T helper type 2 (Th2) anti-inflammatory and Th3 regulatory immune responses. The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the virus that causes Coronavirus disease 2019 (COVID-19), can exacerbate Th1/Th17 pro-inflammatory cytokine production in humans, leading to a cytokine storm. Air pollutants (particulate matter, oxygen radicals, hydrocarbons and volatile organic compounds) and water pollutants (metals and organic chemicals) can also intensify Th1/Th17 immune response and could exacerbate SARS-CoV-2 related respiratory distress and failure. The present review focused on the epidemiology of SARS-CoV-2, helminths and fine particulate matter 2.5 µm or less in diameter (PMKeywords:
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Abstract Severe infection-induced cytokine storm is an urgent medical syndrome with high mortality. To date, no therapy is available. This study shows that high concentrations of lipopolysaccharide (LPS) induce cytokine storm within 48h and thus kill most experimental mice. Rapid, but not late dexamethasone administration remarkably inhibits cytokine storm and rescues LPS-treated mice. Monocytes and macrophages are the major source of cytokine storm. In these cells, pro-inflammatory genes (i.e., Tnf , Il6 and Il1β ) have preassembled RNA polymerase II (RNA Pol II), but stay at the pause stage of transcriptional elongation in the absence of stimulation. LPS rapidly activates transcription of these “pre-loaded” genes within 2h. Administration of dexamethasone within this time window inhibits RNA Pol II ser2 binding to the core promoters of pro-inflammatory genes and thus reduces LPS-induced cytokine transcription. Therefore, rapid utilization of dexamethasone might be efficacious to prevent severe bacterium-induced cytokine storm in clinical practice.
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The terminal stage of Ebola and other viral diseases is often the onset of a cytokine storm, the massive overproduction of cytokines by the body's immune system.The actions of curcumin in suppressing cytokine release and cytokine storm are discussed.Curcumin blocks cytokine release, most importantly the key pro-inflammatory cytokines, interleukin-1, interleukin-6 and tumor necrosis factor-α. The suppression of cytokine release by curcumin correlates with clinical improvement in experimental models of disease conditions where a cytokine storm plays a significant role in mortality.The use of curcumin should be investigated in patients with Ebola and cytokine storm. Intravenous formulations may allow achievement of therapeutic blood levels of curcumin.
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Since December 2019, COVID-19 disease caused by SARS-CoV-2 virus has spread world-wide as pandemic causing large number of infected persons and lot of deaths of COVID patients. There is currently no definite medicine for treatment of the disease as well as any preventive measure. With the progress of multiplication of viruses in the human, activation and amplification of host immune response take place causing massive release of varieties of cytokines like interleukin (IL)-1, IL-6, IL-17, etc., and different types of interferons (IFNs), tumour necrosis factor (TNF) to form cytokine storm. From studies of COVID-19 patients in hospital, it has also been noted that uncontrolled inflammation due to elevated levels of cytokine (cytokine storm) is responsible for causing severity of the disease. In this article the properties of cytokine, types of cytokine and other details have been discussed. The mechanism of signalling of cytokine to immunity and the reason for causing cytokine storm with its role in causing fatalities in COVID 19 patients have also been pointed out. Low infection of virus persists in upper airway that causes similar to seasonal respiratory illness but with severe infections virus remains in the lower respiratory tract leading to lung injury, acute respiratory distress syndrome (ARDS) and sometimes death. The role of cytokine storm in causing severity of disease has been discussed. Key words: Cytokine, IL-6, IL-17, IL-33 families, signalling mechanism, immunity, cytokine storm, role in COVID-19.
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A review Cytokines are a diverse group of small mol proteins or peptides that are secreted by cells for the purpose of intercellular delivery signaling and communication, which play an important role in the immune system by regulating both the intensity and duration of the immune response During infection, the triggering of the inflammatory response, especially through the production of cytokines, is essential for the early elimination of pathogens However, cytokines are intense secreted and released during a hyper inflammatory state that may trigger a dangerous condition known as (or hypercytokinemia), resulting in uncontrolled inflammation in tissues and key organs Cytokine storms are closely related to influenza, sepsis/septic shock and acute respiratory distress syndrome, which ultimately lead to multiple organ failure This review outlines the classification and biol functions of cytokines, the clinic and damage mechanism of cytokine storms, and treatment of 2019 novel coronavirus (2019-nCoV), which provides guidance for the prevention and treatment of cytokine storm syndrome
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Cytokines are a diverse group of small molecule proteins or peptides that are secreted by cells for the purpose of intercellular delivery signaling and communication, which play an important role in the immune system by regulating both the intensity and duration of the immune response During infection, the triggering of the inflammatory response, especially through the production of cytokines, is essential for the early elimination of pathogens However, cytokines are intense secreted and released during a hyperinflammatory state that may trigger a dangerous condition known as (or hypercytokinemia), resulting in uncontrolled inflammation in tissues and key organs Cytokine storms are closely related to influenza, sepsis/septic shock and acute respiratory distress syndrome, which ultimately lead to multiple organ failure This review outlines the classification and biological functions of cytokines, the clinic and damage mechanism of cytokine storms, and treatment of novel coronavirus (SARS-CoV-2), which provides guidance for the prevention and treatment of cytokine storm syndrome
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Cytokine storm is a phenomenon characterized by strong elevated circulating cytokines that most often occur after an overreactive immune system is activated by an acute systemic infection. A variety of cells participate in cytokine storm induction and progression, with profiles of cytokines released during cytokine storm varying from disease to disease. This review focuses on pathophysiological mechanisms underlying cytokine storm induction and progression induced by pathogenic invasive infectious diseases. Strategies for targeted treatment of various types of infection-induced cytokine storms are described from both host and pathogen perspectives. In summary, current studies indicate that cytokine storm-targeted therapies can effectively alleviate tissue damage while promoting the clearance of invading pathogens. Based on this premise, “multi-omics” immune system profiling should facilitate the development of more effective therapeutic strategies to alleviate cytokine storms caused by various diseases.
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Cytokine storm is an excessive immune response that can occur in various medical conditions, including infections, autoimmune diseases, and cancer. It is characterized by a massive release of cytokines, leading to widespread inflammation and tissue damage. Clinical manifestations of cytokine storm include fever, hypotension, respiratory distress, and organ dysfunction. Laboratory findings typically show elevated levels of inflammatory markers and cytokines. The treatment of cytokine storm depends on the underlying cause and severity of the condition, but commonly involves immunosuppressive therapy, cytokine inhibitors, supportive care, plasma exchange, and other therapies. Early recognition and management are crucial for improving patient outcomes. Several cytokine inhibitors have been used in the treatment of cytokine storm, including tocilizumab, anakinra, emapalumab, sarilumab, and baricitinib. However, the use of cytokine inhibitors should be individualized based on the underlying condition and potential side effects. Further research is needed to better understand the pathophysiology of cytokine storm and develop more effective treatment strategies.
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