Novel therapeutic roles for surfactant-inositols and -phosphatidylglycerols in a neonatal piglet ARDS model: a translational study.

@article{Spengler2018NovelTR,
  title={Novel therapeutic roles for surfactant-inositols and -phosphatidylglycerols in a neonatal piglet ARDS model: a translational study.},
  author={Dietmar Spengler and Supandi Winoto-Morbach and Sarah Kupsch and Christina Vock and Katharina Bl{\"o}chle and Susanna Frank and Nele Rintz and Marie Diek{\"o}tter and Harshavardhan Janga and Markus Weckmann and Sabine Fuchs and Andra B. Schromm and Heinz Fehrenbach and Stefan Schütze and Martin F. Krause},
  journal={American journal of physiology. Lung cellular and molecular physiology},
  year={2018},
  volume={314 1},
  pages={
          L32-L53
        }
}
The biological and immune-protective properties of surfactant-derived phospholipids and phospholipid subfractions in the context of neonatal inflammatory lung disease are widely unknown. Using a porcine neonatal triple-hit acute respiratory distress syndrome (ARDS) model (repeated airway lavage, overventilation, and LPS instillation into airways), we assessed whether the supplementation of surfactant (S; poractant alfa) with inositol derivatives [inositol 1,2,6-trisphosphate (IP3) or… 
Role of inositol to improve surfactant functions and reduce IL-6 levels: A potential adjuvant strategy for SARS-CoV-2 pneumonia?
TLDR
Treatment with myo-inositol may be able to reduce IL-6 dependent inflammatory response and improve oxygenation in patients with severe ARDS by SARS-CoV-2.
Inositol and pulmonary function. Could myo-inositol treatment downregulate inflammation and cytokine release syndrome in SARS-CoV-2?
TLDR
Myo-Inositol proved to reduce IL-6 levels in a number of conditions and to mitigate the inflammatory cascade, while being devoid of any significant side effects, and it is tempting to speculate that inositol could be beneficial in managing the most dreadful effects of Sars-CoV-2 infection.
Alveolar lipids in pulmonary disease. A review
TLDR
This work reviews the most recent knowledge on alveolar lipids and their essential metabolic and signaling functions during homeostasis and during some of the most commonly observed pulmonary diseases.
Berberine protects against lipopolysaccharide-induced acute respiratory distress syndrome via sirtuin-1/NF-κB pathway
Objectives: To analyze the effect of berberine on acute respiratory distress syndrome (ARDS) and clarify the underlying mechanism. Background: ARDS is a common respiratory disease. There is no
Crosstalk Between Acid Sphingomyelinase and Inflammasome Signaling and Their Emerging Roles in Tissue Injury and Fibrosis
TLDR
The current understanding of the ASM-ceramide system in inflammasome activation, and how it contributes to multiple diseases is discussed.
Iron and Sphingolipids as Common Players of (Mal)Adaptation to Hypoxia in Pulmonary Diseases
TLDR
This narrative review introduces high altitude pulmonary edema, acute respiratory distress syndrome, Chronic Obstructive Pulmonary Disease, and Cystic Fibrosis as examples of maladaptation to hypoxia, and highlights some of the potential mechanisms influencing the prognosis of the affected patients.
Could natural products modulate early inflammatory responses, preventing acute respiratory distress syndrome in COVID-19-confirmed patients?
TLDR
A systematic review regarding the PANPs that could be further studied as alternatives to prevent ARDS was conducted, allowing their possible use as alternative treatment at the prevention of ARDS in COVID-19-infected or -suspected patients.
Breath-Synchronized Nebulized Surfactant in a Porcine Model of Acute Respiratory Distress Syndrome
TLDR
Breath-synchronized, nebulized bovine surfactant appears to be a safe and feasible treatment option for use in coronavirus disease 2019 and other severe forms of acute respiratory distress syndrome.
An Unsettled Promise: The Newborn Piglet Model of Neonatal Acute Respiratory Distress Syndrome (NARDS). Physiologic Data and Systematic Review
TLDR
The newborn piglet model of acute lung injury serves as an excellent model to study respiratory failure and is the preferred animal model for reasons of availability, body size, similarities of porcine and human lung, robustness, and costs, making the piglet indispensable in anti-inflammatory research.
Lipid–Protein and Protein–Protein Interactions in the Pulmonary Surfactant System and Their Role in Lung Homeostasis
TLDR
This review summarizes some of the most important molecules and interactions within lung surfactant and how multiple lipid–protein and protein–protein interactions contribute to the proper maintenance of an operative respiratory surface.
...
1
2
...

References

SHOWING 1-10 OF 104 REFERENCES
18:1/18:1-Dioleoyl-phosphatidylglycerol prevents alveolar epithelial apoptosis and profibrotic stimulus in a neonatal piglet model of acute respiratory distress syndrome.
TLDR
It is concluded that surfactant fortified by DOPG preserves lung function, and prevents alveolar epithelial injury and fibrous stimulus by reduction of sPLA2 in a neonatal model of acute respiratory distress syndrome without any relevant discernable side effects.
Topical application of phosphatidyl-inositol-3,5-bisphosphate for acute lung injury in neonatal swine
TLDR
Exogenous surfactant “fortified” by PIP2, a naturally occurring surfactants component, improves lung function by topical suppression of aSMase, providing a potential treatment concept for neonates with hypoxemic respiratory failure.
Inositol-trisphosphate reduces alveolar apoptosis and pulmonary edema in neonatal lung injury.
TLDR
It is concluded that the admixture of IP3 to surfactant, but not of Inos, improves gas exchange and edema in the authors' nALI model by the suppression of the governing enzyme aSMase, and that this treatment deserves clinical evaluation.
Improved pulmonary function by acid sphingomyelinase inhibition in a newborn piglet lavage model.
RATIONALE In acute inflammatory lung disease in newborn infants, exogenous surfactant only transiently improves lung function. We hypothesized that the transient nature of this protection is in part
A specific phospholipase C activity regulates phosphatidylinositol levels in lung surfactant of patients with acute respiratory distress syndrome.
TLDR
Evidence of a phosphoinositide-specific phospholipase C (PI-PLC) activity in bronchoalveolar lavage (BAL) fluid, which may regulate PtdIns levels, is presented for the first time.
Secretory Phospholipase A2-Mediated Depletion of Phosphatidylglycerol in Early Acute Respiratory Distress Syndrome
TLDR
The hypothesis that sPLA2-mediated hydrolysis of surfactant phospholipid, especially PG by PLA2G2A, contributes to surfactants injury during early ARDS is supported.
Surfactant “fortification” by topical inhibition of nuclear factor-&kgr;B activity in a newborn piglet lavage model*
TLDR
Supplementation of exogenous surfactant with a NF-&kgr;B inhibitor to create a “fortified” surfactants improves gas exchange, lung function, and pulmonary edema during 24 hrs of mechanical ventilation, without a secondary functional relapse.
Varespladib Inhibits Secretory Phospholipase A2 in Bronchoalveolar Lavage of Different Types of Neonatal Lung Injury
TLDR
Varespladib efficacy was higher in vitro than in lavage fluids obtained from neonates, and sPLA2 activity was reduced in hyaline membrane disease, infections, and meconium aspiration using 40 μM varesPladib.
Topical inhibition of nuclear factor-&kgr;B enhances reduction in lung edema by surfactant in a piglet model of airway lavage
TLDR
A topically applied nuclear factor-&kgr;B inhibitor improves lung edema and lung volumes and reduces inflammation in this newborn piglet model of airway lavage.
Alveolar sphingolipids generated in response to TNF-alpha modifies surfactant biophysical activity.
TLDR
These studies are the first to demonstrate the existence of a cytokine-regulated alveolar pool of sphingomyelin hydrolysis products that impairs the biophysical properties of theAlveolar surfactant film.
...
1
2
3
4
5
...