Yellow Fever–induced Acute Lung Injury

Fabro, Alexandre Todorovic; Engelman, Gustavo Gonçalves; Ferreira, Nilson; Velloni, Júlia Maranhão Fagundes; Espósito, Danillo Lucas Alves; Fonseca, Benedito Antônio Lopes da; Brunaldi, Mariângela Ottoboni

doi:10.1164/rccm.201711-2267im

Cited by 8 publications

(13 citation statements)

References 5 publications

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“…The lung parenchyma was clamped by Collins Forceps, cut, and fixed in 10% buffered formalin. Pulmonary tissue samples were stained with H&E and immunostaining as reported ( Fabro et al, 2015 , 2019 ). The slides were incubated with the primary antibodies, rabbit anti-CD14 mAb (1:200; Abcam), rabbit anti-human NLRP3 mAb (clone D2P5E; 1:3,000; Cell Signaling), and rabbit anti-human ASC polyclonal antibody (1:2,000; Adipogen AL177) for 2 h at room temperature or overnight at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Inflammasomes are activated in response to SARS-CoV-2 infection and are associated with COVID-19 severity in patients

Rodrigues

Sá

Ishimoto

et al. 2020

Journal of Experimental Medicine

Self Cite

683

742

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Severe cases of COVID-19 are characterized by a strong inflammatory process that may ultimately lead to organ failure and patient death. The NLRP3 inflammasome is a molecular platform that promotes inflammation via cleavage and activation of key inflammatory molecules including active caspase-1 (Casp1p20), IL-1β, and IL-18. Although participation of the inflammasome in COVID-19 has been highly speculated, the inflammasome activation and participation in the outcome of the disease are unknown. Here we demonstrate that the NLRP3 inflammasome is activated in response to SARS-CoV-2 infection and is active in COVID-19 patients. Studying moderate and severe COVID-19 patients, we found active NLRP3 inflammasome in PBMCs and tissues of postmortem patients upon autopsy. Inflammasome-derived products such as Casp1p20 and IL-18 in the sera correlated with the markers of COVID-19 severity, including IL-6 and LDH. Moreover, higher levels of IL-18 and Casp1p20 are associated with disease severity and poor clinical outcome. Our results suggest that inflammasomes participate in the pathophysiology of the disease, indicating that these platforms might be a marker of disease severity and a potential therapeutic target for COVID-19.

show abstract

Section: Methodsmentioning

confidence: 99%

Inflammasomes are activated in response to SARS-CoV-2 infection and are associated with COVID-19 severity in patients

Rodrigues

Sá

Ishimoto

et al. 2020

Journal of Experimental Medicine

Self Cite

683

742

View full text Add to dashboard Cite

show abstract

“…The lung parenchyma is clamped by Collins Forceps, cut and fixed in 10% buffered formalin. Pulmonary tissue samples were stained with hematoxylin and eosin (H&E) and immunostaining as reported 18 19 . The slides were incubated with the primary antibodies, rabbit anti-CD14 mAb (Abcam, 1:200) and mouse anti-Nlrp3 mAb (AdipoGen, 1:200), for 2h at room temperature or overnight at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Inflammasome activation in COVID-19 patients

Rodrigues

Ishimoto

et al. 2020

Preprint

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Severe cases of COVID-19 are characterized by a strong inflammatory process that may ultimately lead to organ failure and patient death. The NLRP3 inflammasome is a molecular platform that promotes inflammation via cleavage and activation of key inflammatory molecules including active caspase-1 (Casp1p20), IL-1β and IL-18. Although the participation of the inflammasome in COVID-19 has been highly speculated, the inflammasome activation and participation in the outcome of the disease is unknown. Here we demonstrate that the NLRP3 inflammasome is activated in response to SARS-CoV-2 infection and it is active in COVID-19, influencing the clinical outcome of the disease. Studying moderate and severe COVID-19 patients, we found active NLRP3 inflammasome in PBMCs and tissues of post-mortem patients upon autopsy. Inflammasome-derived products such as Casp1p20 and IL-18 in the sera correlated with the markers of COVID-19 severity, including IL-6 and LDH. Moreover, higher levels of IL-18 and Casp1p20 are associated with disease severity and poor clinical outcome. Our results suggest that the inflammasome is key in the pathophysiology of the disease, indicating this platform as a marker of disease severity and a potential therapeutic target for COVID-19.

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“…Invasive aspergillosis was also reported in a patient following YF vaccine–associated viscerotropic disease 28 . Acute liver failure (ALF) is associated with pro‐inflammatory cytokine overproduction 29 that can lead to microvascular endothelial damage and could explain acute diffuse alveolar injury and rapid progressive respiratory failure in some patients 30,31 . Opportunistic pathogenic fungal coinfections are common in human patients with respiratory viruses where alveolar damage could predispose to AIPA, even in immunocompetent patients 32,33 .…”

Section: Discussionmentioning

confidence: 99%

“…28 Acute liver failure (ALF) is associated with pro-inflammatory cytokine overproduction 29 that can lead to microvascular endothelial damage and could explain acute diffuse alveolar injury and rapid progressive respiratory failure in some patients. 30,31 Opportunistic pathogenic fungal coinfections are common in human patients with respiratory viruses where alveolar damage could predispose to AIPA, even in immunocompetent patients. 32,33 In this case, diffuse alveolar damage was not evident and lung tissue was negative for influenza and YFV.…”

Section: Discussionmentioning

confidence: 99%