Commonalities Between COVID-19 and Radiation Injury

Rios, Carmen; Cassatt, David R.; Hollingsworth, Brynn A.; Satyamitra, Merriline M.; Tadesse, Yeabsera; Taliaferro, Lanyn P.; Winters, Thomas A.; DiCarlo, Andrea L.

doi:10.1667/rade-20-00188.1

Cited by 26 publications

(29 citation statements)

References 328 publications

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“…The SARS-CoV-2 virus causes massive damage to the infected epithelial and endothelial cells, with an excessive release of cytokines and chemokines (18). In SARS-CoV-2, stimulation of the caspase-1 enhances the production of pro-inflammatory cytokines such as IL-1b and IL-6 (24). These cytokines bind with other immune cells, including T-lymphocytes and monocytes (8,25).…”

Section: Inflammation and Sars-cov-2 Infectionmentioning

confidence: 99%

Interplay of Opposing Effects of the WNT/β-Catenin Pathway and PPARγ and Implications for SARS-CoV2 Treatment

Vallée

Lecarpentier²,

Vallée

2021

Front. Immunol.

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The Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), has quickly reached pandemic proportions. Cytokine profiles observed in COVID-19 patients have revealed increased levels of IL-1β, IL-2, IL-6, and TNF-α and increased NF-κB pathway activity. Recent evidence has shown that the upregulation of the WNT/β-catenin pathway is associated with inflammation, resulting in a cytokine storm in ARDS (acute respire distress syndrome) and especially in COVID-19 patients. Several studies have shown that the WNT/β-catenin pathway interacts with PPARγ in an opposing interplay in numerous diseases. Furthermore, recent studies have highlighted the interesting role of PPARγ agonists as modulators of inflammatory and immunomodulatory drugs through the targeting of the cytokine storm in COVID-19 patients. SARS-CoV2 infection presents a decrease in the angiotensin-converting enzyme 2 (ACE2) associated with the upregulation of the WNT/β-catenin pathway. SARS-Cov2 may invade human organs besides the lungs through the expression of ACE2. Evidence has highlighted the fact that PPARγ agonists can increase ACE2 expression, suggesting a possible role for PPARγ agonists in the treatment of COVID-19. This review therefore focuses on the opposing interplay between the canonical WNT/β-catenin pathway and PPARγ in SARS-CoV2 infection and the potential beneficial role of PPARγ agonists in this context.

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Section: Inflammation and Sars-cov-2 Infectionmentioning

confidence: 99%

Interplay of Opposing Effects of the WNT/β-Catenin Pathway and PPARγ and Implications for SARS-CoV2 Treatment

Vallée

Lecarpentier²,

Vallée

2021

Front. Immunol.

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“…Rapid viral replication can result in increased pyroptosis, which can be a precursor for massive release of inflammatory mediators. 10 In COVID-19, uncontrolled immune response can lead to secondary hemophagocytic lympho-histiocytosis or macrophage activation syndrome, which presents as a lifethreatening condition, in the form of persistent fever and pancytopenia quickly progressing into multi-organ failure and increased mortality. 11,12 Macrophage activation syndrome is diagnosed on the basis of clinical and laboratory diagnostic criteria which include fever, increased ferritin, triglyceride levels, pancytopenia, consumptive coagulopathy with hypofibrinogenemia, and splenomegaly.…”

Section: Cytokine Storm and Immune Activation In Covid-19mentioning

confidence: 99%

“…The presentation of viral antigens using the major histocompatibility complex ensures activation of both the innate and acquired immunity, resulting in proinflammatory cytokines, chemokines, and coagulation enzymes. 9 , 10 These inflammatory pathways, if dysregulated result in massive activation and ‘cytokine storm’, a prothrombotic tendency culminating into multiple organ failures and likely death. Pyroptosis is a form of programmed cell death which is an inflammatory caspase-1 dependent type, that occurs in response to infection with intracellular pathogens, such as SARS-CoV-2.…”

Section: Cytokine Storm and Immune Activation In Covid-19mentioning

confidence: 99%

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Cytokine Storm of COVID-19 and its Impact on Patients with and without Chronic Liver Disease

Premkumar¹,

Kedarisetty²

2021

Journal of Clinical and Translational Hepatology

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The coronavirus pandemic has resulted in increased rates of hepatic decompensation, morbidity and mortality in patients suffering from existing liver disease, and deranged liver biochemistries in those without liver disease. In patients with cirrhosis with coronavirus disease 2019 (COV-ID-19), new onset organ failures manifesting as acute-onchronic liver failure have also been reported. The severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) also directly binds to enterocytes and cholangiocytes via the angiotensin converting enzyme receptor 2, although the lung remains the portal of entry. Superadded with the COVID-19 related bystander hepatitis, a systemic inflammatory response is noted due to unregulated macrophage activation syndrome and cytokine storm. However, the exact definition and diagnostic criteria of the 'cytokine storm' in COVID-19 are yet unclear. In addition, inflammatory markers like C-reactive protein, ferritin, D-dimer and procalcitonin are frequently elevated. This in turn leads to disease progression, activation of the coagulation cascade, vascular microthrombi and immune-mediated injury in different organ systems. Deranged liver chemistries are also noted due to the cytokine storm, and synergistic hypoxic or ischemic liver injury, drug-induced liver injury, and use of hepatotoxic antiviral agents all contribute to deranged liver chemistry. Control of an unregulated cytokine storm at an early stage may avert disease morbidity and mortality. Several immunomodulator drugs and repurposed immunosuppressive agents have been used in COVID-19 with varying degrees of success.

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“…Various observations point towards an interplay of multiple factors in the pathogenesis of COVID-19 induced cytokine storm syndrome. Several studies have drawn parallels between the pathophysiology of cytokine storm syndrome in severe COVID-19 and the acute radiation syndrome (ARS) with inflammation being the common key player (Rios et al, 2021). Cytokine storm has been characterized by the elevated serum levels of the following cytokines and chemokines such as interleukin-1b (IL-1 b), IL-2, IL-7, IL-8, IL-9, IL-10, granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), Interferon-gamma (IFN-g), tumor necrosis factor-alpha (TNF-a), IFN-g-inducible protein-10 (IP-10), monocyte chemoattractant protein-1 (MCP1) and macrophage inflammatory protein-1 A (MIP1A) (Wu and Yang, 2020).…”

Section: Foraying Through the Eye Of Cytokine Stormmentioning

confidence: 99%

Could Nutraceutical Approaches Possibly Attenuate the Cytokine Storm in COVID-19 Patients?

Vignesh

Velu

Sureban

2021

Front. Cell. Infect. Microbiol.

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Commonalities Between COVID-19 and Radiation Injury

Cited by 26 publications

References 328 publications

Interplay of Opposing Effects of the WNT/β-Catenin Pathway and PPARγ and Implications for SARS-CoV2 Treatment

Interplay of Opposing Effects of the WNT/β-Catenin Pathway and PPARγ and Implications for SARS-CoV2 Treatment

Cytokine Storm of COVID-19 and its Impact on Patients with and without Chronic Liver Disease

Could Nutraceutical Approaches Possibly Attenuate the Cytokine Storm in COVID-19 Patients?

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