Inflammatory Response in COVID-19 Patients Resulting from the Interaction of the Inflammasome and SARS-CoV-2

Cheon, So Yeong; Koo, Bon‐Nyeo

doi:10.3390/ijms22157914

Cited by 17 publications

(10 citation statements)

References 61 publications

(133 reference statements)

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“…Together with other cytokines, increased expression of IL-18 contributes to macrophage activation syndrome, a condition seen in autoimmune diseases and influenza. Previous studies revealed similarities in the pathogenesis of COVID-19 and macrophage activation syndrome [ 3 , 12 ].…”

Section: Discussionmentioning

confidence: 99%

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Elevated IL-18 Predicts Poor Prognosis in Critically ill COVID-19 Patients at a Brazilian Hospital in 2020–21

et al. 2022

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Background: A dysregulated inflammatory response contributes to decline in patients with COVID-19. This cross-sectional study evaluated biomarkers of unvaccinated patients admitted to the intensive care unit of a hospital in Fortaleza, Brazil. Methods: Twenty cytokines were quantified upon hospital admission; clinical and laboratory data were analyzed, as well as sociodemographic data, to search for an association with clinical outcomes, including fatal (n = 40) or recovered cases (n = 38). Results: Fatal cases exhibited significantly higher levels of IL-18 (p = 0.009); deceased patients were older (p = 0.0001), had a lower number of platelets (p = 0.0063) and higher neutrophil–lymphocyte ratio (p = 0.0230) than those who recovered. Conclusion: These findings indicate that IL-18 is a possible marker to predict poor prognosis in critically ill patients with COVID-19.

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Section: Discussionmentioning

confidence: 99%

“…When this process is overactivated, exacerbated inflammation triggers the disease aggravation. Studies show that NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome is highly expressed in patients with COVID-19, being a potential marker of disease severity [ 11 , 12 ].…”

Section: Discussionmentioning

confidence: 99%

Elevated IL-18 Predicts Poor Prognosis in Critically ill COVID-19 Patients at a Brazilian Hospital in 2020–21

et al. 2022

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“…As a basis of the pulmonary inflammatory response, it was postulated that lung epithelial cells could express the NLRP3 inflammasome, which was identified as one of the most detrimental signaling molecules in lung inflammatory conditions [ 52 , 53 ]. Moreover, NLRP3 is known to coordinate the uncontrolled inflammatory pathway referred to as the NLRP3 inflammasome.…”

Section: Discussionmentioning

confidence: 99%

Hesperetin from Root Extract of Clerodendrum petasites S. Moore Inhibits SARS-CoV-2 Spike Protein S1 Subunit-Induced NLRP3 Inflammasome in A549 Lung Cells via Modulation of the Akt/MAPK/AP-1 Pathway

Arjsri

Srisawad

Mapoung

et al. 2022

IJMS

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Inhibition of inflammatory responses from the spike glycoprotein of SARS-CoV-2 (Spike) by targeting NLRP3 inflammasome has recently been developed as an alternative form of supportive therapy besides the traditional anti-viral approaches. Clerodendrum petasites S. Moore (C. petasites) is a Thai traditional medicinal plant possessing antipyretic and anti-inflammatory activities. In this study, C. petasites ethanolic root extract (CpEE) underwent solvent-partitioned extraction to obtain the ethyl acetate fraction of C. petasites (CpEA). Subsequently, C. petasites extracts were determined for the flavonoid contents and anti-inflammatory properties against spike induction in the A549 lung cells. According to the HPLC results, CpEA significantly contained higher amounts of hesperidin and hesperetin flavonoids than CpEE (p < 0.05). A549 cells were then pre-treated with either C. petasites extracts or its active flavonoids and were primed with 100 ng/mL of spike S1 subunit (Spike S1) and determined for the anti-inflammatory properties. The results indicate that CpEA (compared with CpEE) and hesperetin (compared with hesperidin) exhibited greater anti-inflammatory properties upon Spike S1 induction through a significant reduction in IL-6, IL-1β, and IL-18 cytokine releases in A549 cells culture supernatant (p < 0.05). Additionally, CpEA and hesperetin significantly inhibited the Spike S1-induced inflammatory gene expressions (NLRP3, IL-1β, and IL-18, p < 0.05). Mechanistically, CpEA and hesperetin attenuated inflammasome machinery protein expressions (NLRP3, ASC, and Caspase-1), as well as inactivated the Akt/MAPK/AP-1 pathway. Overall, our findings could provide scientific-based evidence to support the use of C. petasites and hesperetin in the development of supportive therapies for the prevention of COVID-19-related chronic inflammation.

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“…In the COVID-19 pandemic, some evidence supports the involvement of inflammasomes in SARS-CoV-2-derived interstitial fibrosis and diffuse alveolar damage [ 106 ]. Moreover, SARS-CoV-2 might directly activate the NLRP3 inflammasome, resulting in the activation of macrophages, neutrophil infiltration, reduced apoptosis and excessive cytokine production which can lead to cytokine storms and fibrosis [ 107 ].…”

Section: Potential Mechanism Of Virus Infection-induced Damage That Associated With the Nlrp3 Inflammasomementioning

confidence: 99%

The Crucial Role of NLRP3 Inflammasome in Viral Infection-Associated Fibrosing Interstitial Lung Diseases

Effendi

Nagano

2021

IJMS

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Idiopathic pulmonary fibrosis (IPF), one of the most common fibrosing interstitial lung diseases (ILD), is a chronic-age-related respiratory disease that rises from repeated micro-injury of the alveolar epithelium. Environmental influences, intrinsic factors, genetic and epigenetic risk factors that lead to chronic inflammation might be implicated in the development of IPF. The exact triggers that initiate the fibrotic response in IPF remain enigmatic, but there is now increasing evidence supporting the role of chronic exposure of viral infection. During viral infection, activation of the NLRP3 inflammasome by integrating multiple cellular and molecular signaling implicates robust inflammation, fibroblast proliferation, activation of myofibroblast, matrix deposition, and aberrant epithelial-mesenchymal function. Overall, the crosstalk of the NLRP3 inflammasome and viruses can activate immune responses and inflammasome-associated molecules in the development, progression, and exacerbation of IPF.

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Inflammatory Response in COVID-19 Patients Resulting from the Interaction of the Inflammasome and SARS-CoV-2

Cited by 17 publications

References 61 publications

Elevated IL-18 Predicts Poor Prognosis in Critically ill COVID-19 Patients at a Brazilian Hospital in 2020–21

Elevated IL-18 Predicts Poor Prognosis in Critically ill COVID-19 Patients at a Brazilian Hospital in 2020–21

Hesperetin from Root Extract of Clerodendrum petasites S. Moore Inhibits SARS-CoV-2 Spike Protein S1 Subunit-Induced NLRP3 Inflammasome in A549 Lung Cells via Modulation of the Akt/MAPK/AP-1 Pathway

The Crucial Role of NLRP3 Inflammasome in Viral Infection-Associated Fibrosing Interstitial Lung Diseases

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