Cytokine Profiles as Potential Prognostic and Therapeutic Markers in SARS-CoV-2-Induced ARDS

Salton, Francesco; Confalonieri, Paola; Campisciano, Giuseppina; Cifaldi, Rossella; Rizzardi, Clara; Generali, Daniele; Pozzan, Riccardo; Tavano, Stefano; Bozzi, Chiara; Lapadula, Giulia; Meduri, G. Umberto; Confalonieri, Marco; Comar, Manola; Lerda, Selene; Ruaro, Barbara

doi:10.3390/jcm11112951

Cited by 51 publications

(90 citation statements)

References 23 publications

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“…Furthermore, the role and regulation that the cytoskeleton plays in the fusion of the lamellar body to the plasma membrane and in the recycling of surfactant material, and the identification of the molecular mechanisms that couple the rate of recycling to the rate of secretion, are still debated. These important issues must be better understood if we are to clarify how surfactant secretion and recycling are regulated [11][12][13]. Surfactant lipids have both hydrophilic and hydrophobic properties (amphipathy), and the head groups have charged qualities that form stable, surface-active films at the air-liquid alveolar interface.…”

Section: Production and Secretion Of Surfactant By Atii Pneumocytesmentioning

confidence: 99%

“…Surfactant lipids have both hydrophilic and hydrophobic properties (amphipathy), and the head groups have charged qualities that form stable, surface-active films at the air-liquid alveolar interface. The low surface tension is provided by phospholipids, predominantly dipalmitoylphosphatidylcholine, and it is assisted by the hydrophobic surfactant proteins SP-B and SP-C [11][12][13]. As only ATII cells produce the surfactant protein C, it is considered an ATII cell-specific marker.…”

Section: Production and Secretion Of Surfactant By Atii Pneumocytesmentioning

confidence: 99%

“…As only ATII cells produce the surfactant protein C, it is considered an ATII cell-specific marker. Moreover, pulmonary surfactant protects the distal lung from noxious particles and microorganisms [11][12][13]. This surfactant resides on top of a thin water layer that covers the inner surface of the alveoli.…”

Section: Production and Secretion Of Surfactant By Atii Pneumocytesmentioning

confidence: 99%

“…COVID-19 causes both pneumonia and acute respiratory distress syndrome (ARDS) [3][4][5][6][7]. The SARS-CoV-2 virus uses the angiotensin-converting enzyme 2 (ACE2) receptor, in conjunction with serine protease TMPRSS2, expressed by alveolar type II (ATII) cells, as one of the SARS-CoV-2 target cells, to enter into the ATII pneumocytes [8][9][10][11][12]. After ATII infection and the resulting damage, the consequences may be severe and may include injury to the alveolar-capillary barrier, lung edema, inflammation, ineffective gas exchange, impaired lung mechanics, and reduced oxygenation, which resembles COVID-19 acute respiratory distress syndrome (COVID-19 ARDS) [10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

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Severe COVID-19 ARDS Treated by Bronchoalveolar Lavage with Diluted Exogenous Pulmonary Surfactant as Salvage Therapy: In Pursuit of the Holy Grail?

Ruaro

Confalonieri

Pozzan

et al. 2022

JCM

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Background: Severe pneumonia caused by coronavirus disease 2019 (COVID-19) is characterized by inflammatory lung injury, progressive parenchymal stiffening and consolidation, alveolar and airway collapse, altered vascular permeability, diffuse alveolar damage, and surfactant deficiency. COVID-19 causes both pneumonia and acute respiratory distress syndrome (COVID-19 ARDS). COVID-19 ARDS is characterized by severe refractory hypoxemia and high mortality. Despite extensive research, the treatment of COVID-19 ARDS is far from satisfactory. Some treatments are recommended for exhibiting some clinically positive impacts on COVID-19 patients although there are already several drugs in clinical trials, some of which are already demonstrating promising results in addressing COVID-19. Few studies have demonstrated beneficial effects in non-COVID-19 ARDS treatment of exogenous surfactant, and there is no evidence-based, proven method for the procedure of surfactant administration. Aim: The aim of this work is to underline the key role of ATII cells and reduced surfactant levels in COVID-19 ARDS and to emphasize the rational basis for exogenous surfactant therapy in COVID-19 ARDS, providing insights for future research. Methods: In this article, we describe and support via the literature the decision to administer large volumes of surfactant to two patients via bronchoalveolar lavage to maximize its distribution in the respiratory tract. Results: In this study, we report on two cases of COVID-19 ARDS in patients who have been successfully treated with diluted surfactants by bronchoalveolar lavage, followed by a low-dose bolus of surfactant. Conclusion: Combining the administration of diluted, exogenous pulmonary surfactant via bronchoalveolar lavage along with the standard therapy for SARS-COV-2-induced ARDS may be a promising way of improving the management of ARDS.

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Section: Production and Secretion Of Surfactant By Atii Pneumocytesmentioning

confidence: 99%

Section: Production and Secretion Of Surfactant By Atii Pneumocytesmentioning

confidence: 99%

Section: Production and Secretion Of Surfactant By Atii Pneumocytesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Severe COVID-19 ARDS Treated by Bronchoalveolar Lavage with Diluted Exogenous Pulmonary Surfactant as Salvage Therapy: In Pursuit of the Holy Grail?

Ruaro

Confalonieri

Pozzan

et al. 2022

JCM

Self Cite

View full text Add to dashboard Cite

show abstract

“…Medicina 2022, 58, 842 2 of 8 to invasive mechanical ventilation (IMV) is associated with significantly higher morbidity and mortality [4].…”

Section: Introductionmentioning

confidence: 99%

Elevated Transaminases as Predictors of COVID-19 Pneumonia Severity

et al. 2022

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Background: This study aimed to calculate the frequency of elevated liver enzymes in hospitalized patients with coronavirus disease 2019 (COVID-19) infection and to test if liver enzyme biochemistry levels on admission could predict the computed tomography (CT) scan severity score of bilateral interstitial pneumonia. Methods: This single-center study comprised of 323 patients including their demographic data, laboratory analyses, and radiological findings. All the information was taken from electronic health records, followed by statistical analysis. Results: Out of 323 patients, 115 of them (35.60%) had aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT) over 40 U/L on admission. AST was the best predictor of CT scan severity score of bilateral interstitial pneumonia (R2 = 0.313, Adjusted R2 = 0.299). CT scan severity score in the peak of the infection could be predicted with the value of AST, neutrophils, platelets, and monocytes count (R2 = 0.535, Adjusted R2 = 0.495). Conclusion: AST, neutrophils, platelets, and monocytes count on admission can account for almost half (49.5%) of the variability in CT scan severity score at peak of the disease, predicting the extensiveness of interstitial pneumonia related to COVID-19 infection. Liver enzymes should be closely monitored in order to stratify COVID-19 patients with a higher risk of developing severe forms of the disease and to plan the beforehand step-up treatment.

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The effect of Fingolimod on patients with moderate to severe COVID‐19

Teymouri

Kaleybar

Hejazian

et al. 2022

Pharmacology Res & Perspec

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Hyper‐inflammation, cytokine storm, and recruitment of immune cells lead to uncontrollable endothelial cell damage in patients with coronavirus disease 2019 (COVID‐19). Sphingosine 1‐phosphate (S1P) signaling is needed for endothelial integrity and its decreased serum level is a predictor of clinical severity in COVID‐19. In this clinical trial, the effect of Fingolimod, an agonist of S1P, was evaluated on patients with COVID‐19. Forty patients with moderate to severe COVID‐19 were enrolled and divided into two groups including (1) the control group ( n = 21) receiving the national standard regimen for COVID‐19 patients and (2) the intervention group ( n = 19) that prescribed daily Fingolimod (0.5 mg) for 3 days besides receiving the standard national regimen for COVID‐19. The hospitalization period, re‐admission rate, intensive care unit (ICU) administration, need for mechanical ventilation, and mortality rate were assessed as primary outcomes in both groups. The results showed that re‐admission was significantly decreased in COVID‐19 patients who received Fingolimod compared to the controls ( p = .04). In addition, the hemoglobin levels of the COVID‐19 patients in the intervention group were increased compared to the controls ( p = .018). However, no significant differences were found regarding the intubation or mortality rate between the groups ( p > .05). Fingolimod could significantly reduce the re‐admission rate after hospitalization with COVID‐19. Fingolimod may not enhance patients' outcomes with moderate COVID‐19. It is necessary to examine these findings in a larger cohort of patients with severe to critical COVID‐19.

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Cytokine Profiles as Potential Prognostic and Therapeutic Markers in SARS-CoV-2-Induced ARDS

Cited by 51 publications

References 23 publications

Severe COVID-19 ARDS Treated by Bronchoalveolar Lavage with Diluted Exogenous Pulmonary Surfactant as Salvage Therapy: In Pursuit of the Holy Grail?

Severe COVID-19 ARDS Treated by Bronchoalveolar Lavage with Diluted Exogenous Pulmonary Surfactant as Salvage Therapy: In Pursuit of the Holy Grail?

Elevated Transaminases as Predictors of COVID-19 Pneumonia Severity

The effect of Fingolimod on patients with moderate to severe COVID‐19

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