Endothelial Protein C Receptor Could Contribute to Experimental Malaria-Associated Acute Respiratory Distress Syndrome

Ortolan, Luana dos Santos; Sercundes, Michelle Klein; Moura, Gabriel Cândido; Quirino, Thatyane de Castro; Debone, Daniela; Costa, Douglas de Sousa; Murillo, Oscar; Marinho, Cláudio Romero Farias; Epiphânio, Sabrina

doi:10.1101/348318

Cited by 3 publications

(2 citation statements)

References 57 publications

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“…ACE2 downregulation impacts the RAS-KKS system resulting in coagulation disturbances, and increases the chances of thrombosis and microthrombosis ( 10 , 11 ). In malaria, the acute respiratory distress syndrome also presents competitive binding of other surface proteins, such as Endothelial Protein C Receptor (EPCR), that when cleaves its ligand PAR-1, inhibits NFκB activation, reducing overall local inflammation ( 51 ). It is currently not known if SARS-CoV-2 infection results in downregulation of those same surface proteins, resulting in higher inflammatory response.…”

Section: Systemic Inflammatory Response Induced By Lung Inflammationmentioning

confidence: 99%

Overview: Systemic Inflammatory Response Derived From Lung Injury Caused by SARS-CoV-2 Infection Explains Severe Outcomes in COVID-19

Polidoro

Hagan

Santiago³

et al. 2020

Front. Immunol.

153

149

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Most SARS-CoV2 infections will not develop into severe COVID-19. However, in some patients, lung infection leads to the activation of alveolar macrophages and lung epithelial cells that will release proinflammatory cytokines. IL-6, TNF, and IL-1β increase expression of cell adhesion molecules (CAMs) and VEGF, thereby increasing permeability of the lung endothelium and reducing barrier protection, allowing viral dissemination and infiltration of neutrophils and inflammatory monocytes. In the blood, these cytokines will stimulate the bone marrow to produce and release immature granulocytes, that return to the lung and further increase inflammation, leading to acute respiratory distress syndrome (ARDS). This lung-systemic loop leads to cytokine storm syndrome (CSS). Concurrently, the acute phase response increases the production of platelets, fibrinogen and other pro-thrombotic factors. Systemic decrease in ACE2 function impacts the Renin-Angiotensin-Kallikrein-Kinin systems (RAS-KKS) increasing clotting. The combination of acute lung injury with RAS-KKS unbalance is herein called COVID-19 Associated Lung Injury (CALI). This conservative two-hit model of systemic inflammation due to the lung injury allows new intervention windows and is more consistent with the current knowledge.

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Section: Systemic Inflammatory Response Induced By Lung Inflammationmentioning

confidence: 99%

Overview: Systemic Inflammatory Response Derived From Lung Injury Caused by SARS-CoV-2 Infection Explains Severe Outcomes in COVID-19

Polidoro

Hagan

Santiago³

et al. 2020

Front. Immunol.

153

149

View full text Add to dashboard Cite

show abstract

“…Ortolan et al found through research that the change of endothelial protein C receptor is an important risk factor in the pathogenesis of acute respiratory distress syndrome. Using protein monitoring technology, they learned that the change of endothelial protein C receptor will increase cell adhesion, and the improvement of cell adhesion is the main influencing factor of acute respiratory distress syndrome [23]. In order to understand the pathogenesis of acute respiratory distress syndrome, Dahmer et al found that the increase of surfactant protein D is a relatively specific indicator of lung injury through protein monitoring and proved that the increase of surfactant protein D is related to the poor prognosis of children with acute respiratory failure through the design of relevant experiments [24].…”

Section: Acute Respiratory Distress Syndrome Protein Monitoringmentioning

confidence: 99%

Dynamic Monitoring of Serum Protein in Acute Respiratory Distress Syndrome Based on Artificial Neural Network

Zhou

Long

2022

Computational and Mathematical Methods in Medicine

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Acute respiratory distress syndrome (ARDS) is one of the more serious diseases in human lung disease. Reducing its incidence rate is an important task in current clinical research. Dynamic monitoring of serum protein in patients will help to achieve the early diagnosis and treatment of ARDS. In this study, a protein monitoring model based on artificial neural network is proposed. First, surface enhanced laser desorption ionization time-of-flight mass spectrometry is used for protein detection, and then BP neural network is used for protein classification and content analysis. In the experimental analysis, serum samples from patients with acute respiratory distress syndrome in our hospital from November 2020 to August 2021 were selected for experimental testing. The experimental results show that the serum protein monitoring model based on BP neural network has low error and high convergence ability and can monitor individual protein in protein monitoring, and the area under the ROC curve in diagnostic performance reaches 0.854. The above results show that the artificial neural network has a good effect on the dynamic monitoring of serum protein in acute respiratory distress syndrome, and the diagnostic performance evaluation can reach 0.854, which has the ability to significantly improve the clinical diagnosis and treatment of acute respiratory distress syndrome.

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The IL-33/ST2 Axis in Immune Responses Against Parasitic Disease: Potential Therapeutic Applications

Ryan

Anderson

Volpedo

et al. 2020

Front. Cell. Infect. Microbiol.

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Parasitic infections pose a wide and varying threat globally, impacting over 25% of the global population with many more at risk of infection. These infections are comprised of, but not limited to, toxoplasmosis, malaria, leishmaniasis and any one of a wide variety of helminthic infections. While a great deal is understood about the adaptive immune response to each of these parasites, there remains a need to further elucidate the early innate immune response. Interleukin-33 is being revealed as one of the earliest players in the cytokine milieu responding to parasitic invasion, and as such has been given the name "alarmin." A nuclear cytokine, interleukin-33 is housed primarily within epithelial and fibroblastic tissues and is released upon cellular damage or death. Evidence has shown that interleukin-33 seems to play a crucial role in priming the immune system toward a strong T helper type 2 immune response, necessary in the clearance of some parasites, while disease exacerbating in the context of others. With the possibility of being a double-edged sword, a great deal remains to be seen in how interleukin-33 and its receptor ST2 are involved in the immune response different parasites elicit, and how those parasites may manipulate or evade this host mechanism. In this review article we compile the current cutting-edge research into the interleukin-33 response to toxoplasmosis, malaria, leishmania, and helminthic infection. Furthermore, we provide insight into directions interleukin-33 research may take in the future, potential immunotherapeutic applications of interleukin-33 modulation and how a better clarity of early innate immune system responses involving interleukin-33/ST2 signaling may be applied in development of much needed treatment options against parasitic invaders.

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Endothelial Protein C Receptor Could Contribute to Experimental Malaria-Associated Acute Respiratory Distress Syndrome

Abstract: 18 Br Li Ki Lu He

Cited by 3 publications

References 57 publications

Overview: Systemic Inflammatory Response Derived From Lung Injury Caused by SARS-CoV-2 Infection Explains Severe Outcomes in COVID-19

Overview: Systemic Inflammatory Response Derived From Lung Injury Caused by SARS-CoV-2 Infection Explains Severe Outcomes in COVID-19

Dynamic Monitoring of Serum Protein in Acute Respiratory Distress Syndrome Based on Artificial Neural Network

The IL-33/ST2 Axis in Immune Responses Against Parasitic Disease: Potential Therapeutic Applications

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