Surfactant Components and Tracheal Aspirate Inflammatory Markers in Preterm Infants with Respiratory Distress Syndrome

Verlato, Giovanna; Simonato, Manuela; Giambelluca, Sonia; Fantinato, Margherita; Correani, Alessio; Cavicchiolo, Maria Elena; Priante, Elena; Carnielli, Virgilio P.; Cogo, Paola

doi:10.1016/j.jpeds.2018.08.019

Cited by 13 publications

(11 citation statements)

References 36 publications

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“…RDS is a respiratory disorder that mostly affects preterm infants and it is characterised by lung immaturity and critically low amounts of pulmonary surfactant [1, 2]. To overcome pulmonary surfactant deficiency, exogenous surfactant replacement therapy represents a crucial achievement in the care of the preterm newborn [3], reducing death and pneumothorax [4].…”

Section: Introductionmentioning

confidence: 99%

Tracing exogenous surfactant in vivo in rabbits by the natural variation of 13C

et al. 2019

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Background Respiratory Distress Syndrome (RDS) is a prematurity-related breathing disorder caused by a quantitative deficiency of pulmonary surfactant. Surfactant replacement therapy is effective for RDS newborns, although treatment failure has been reported. The aim of this study is to trace exogenous surfactant by 13 C variation and estimate the amount reaching the lungs at different doses of the drug. Methods Forty-four surfactant-depleted rabbits were obtained by serial bronchoalveolar lavages (BALs), that were merged into a pool (BAL pool) for each animal. Rabbits were in nasal continuous positive airway pressure and treated with 0, 25, 50, 100 or 200 mg/kg of poractant alfa by InSurE. After 90 min, rabbits were depleted again and a new pool (BAL end experiment) was collected. Disaturated-phosphatidylcholine (DSPC) was measured by gas chromatography. DSPC-Palmitic acid (PA) 13 C/ 12 C was analyzed by isotope ratio mass spectrometry. One-way non-parametric ANOVA and post-hoc Dunn’s multiple comparison were used to assess differences among experimental groups. Results Based on DSPC-PA 13 C/ 12 C in BAL pool and BAL end experiment, the estimated amount of exogenous surfactant ranged from 61 to 87% in dose-dependent way ( p < 0.0001) in animals treated with 25 up to 200 mg/kg. Surfactant administration stimulated endogenous surfactant secretion. The percentage of drug recovered from lungs did not depend on the administered dose and accounted for 31% [24–40] of dose. Conclusions We reported a risk-free method to trace exogenous surfactant in vivo. It could be a valuable tool for assessing, alongside the physiological response, the delivery efficiency of surfactant administration techniques.

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Section: Introductionmentioning

confidence: 99%

Tracing exogenous surfactant in vivo in rabbits by the natural variation of 13C

et al. 2019

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“…Besides, it can alleviate oxidative stress and enhance immunity in the process of inflammation (Kertys, Grendar, Kosutova, Mokra, & Mokry, 2020). A previous study has confirmed that PC was strongly damaged in the lungs of newborns diagnosed with pneumonia and its concentration was decreased in the plasma of adults with CAP (Arshad et al, 2019;Verlato et al, 2018). In our study, the plasma levels of PC (20:4_20:4) and PC (18:1_18:1) were decreased in HS compared with CS, reflecting the lung injury in pediatric CAP (Table S3).…”

Section: Discussionmentioning

confidence: 97%

Plasma characteristic metabolites of pediatric community‐acquired pneumonia in traditional Chinese medicine syndrome differentiation

Lin

Shouchuan

et al. 2021

The Anatomical Record

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Community-acquired pneumonia (CAP) is the leading cause of lower respiratory tract infections in children. Heat syndrome (HS) and cold syndrome (CS) are two main syndrome types of pediatric CAP in traditional Chinese medicine (TCM). This study aimed to identify plasma metabolic profiles in pediatric CAP and to further select potential biomarkers to distinguish between HS and CS. An ultra-performance liquid chromatography coupled with linear ion trap quadrupole-orbitrap mass spectrometry method was applied to plasma samples of 296 patients and 55 healthy controls (HC).The samples were divided into the discovery group (n = 213, HS = 160, CS = 23, HC = 30) and the validation group (n = 138, HS = 93, CS = 20, HC = 25). The orthogonal partial least-squares discriminant analysis, the value of fold change, and Kruskal-Wallis test with false discovery rate correction (q-value <0.05) were applied to identify differential plasma metabolites.The area under the ROC curve (AUC) was used to evaluate the diagnostic performance of the screened metabolites. The results showed that the plasma levels of aspartic acid, phenylalanine, arginine, lysoPC20:1, lysoPE16:0, lysoPE18:0, and PE (16:0_22:6) were increased in CS compared with HC. The plasma levels of PC (18:1_18:1), PC (20:4_20:4), PE (16:0_18:2), lysoPE20:4, lysoPE18:2, and lysoPE22:6 were decreased, whereas, the plasma level of ceramide (d18:1_24:1) was increased in HS compared with HC. There were 13 differential metabolites in CS (AUC = 0.995) and 15 differential metabolites in HS (AUC = 0.954), compared with HC. A panel of seven biomarkers, including LysoPC20:1, lysoPE16:0, lysoPE18:2, lysoPE20:4, lysoPE22:6, PC (18:1_18:1), and PC (20:4_20:4) showed good discrimination between HS and CS with an AUC of 0.982. Altered plasma amino acids and lipids may provide an objective basis for TCM syndrome differentiation in pediatric CAP.

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“…Mice infected with influenza virus have shown lower amounts of phosphatidylcholine and alters the metabolism of PS, which are attributed to the development of ARDS (Woods et al, 2016). The effects of SP deficiencies or dysfunctions is paramount in the pathogenesis of neonatal respiratory diseases (Verlato et al, 2018). In neonates, SP-A is critical in lung immune system while SP-B is important in sustaining respiratory physiology.…”

Section: Pulmonary Surfactant Deficiency/ Dysfunctionmentioning

confidence: 99%

“…The effects of SP deficiencies or dysfunctions is paramount in the pathogenesis of neonatal respiratory diseases ( Verlato et al, 2018 ). In neonates, SP-A is critical in lung immune system while SP-B is important in sustaining respiratory physiology.…”

Section: Pulmonary Surfactant Deficiency/dysfunctionmentioning

confidence: 99%

The Role of Pulmonary Surfactants in the Treatment of Acute Respiratory Distress Syndrome in COVID-19

Wang

et al. 2021

Front. Pharmacol.

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Lung alveolar type-II (AT-II) cells produce pulmonary surfactant (PS), consisting of proteins and lipids. The lipids in PS are primarily responsible for reducing the air-fluid surface tension inside the alveoli of the lungs and to prevent atelectasis. The proteins are of two types: hydrophilic and hydrophobic. Hydrophilic surfactants are primarily responsible for opsonisation, thereby protecting the lungs from microbial and environmental contaminants. Hydrophobic surfactants are primarily responsible for respiratory function. Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) enters the lungs through ACE-2 receptors on lungs and replicates in AT-II cells leading to the etiology of Coronavirus disease – 2019 (COVID-19). The SARS-CoV-2 virus damages the AT-II cells and results in decreased production of PS. The clinical symptoms of acute respiratory distress syndrome (ARDS) in COVID-19 patients are like those of neonatal respiratory distress syndrome (NRDS). The PS treatment is first-line treatment option for NRDS and found to be well tolerated in ARDS patients with inconclusive efficacy. Over the past 70°years, a lot of research is underway to produce natural/synthetic PS and developing systems for delivering PS directly to the lungs, in addition to finding the association between PS levels and respiratory illnesses. In the present COVID-19 pandemic situation, the scientific community all over the world is searching for the effective therapeutic options to improve the clinical outcomes. With a strong scientific and evidence-based background on role of PS in lung homeostasis and infection, few clinical trials were initiated to evaluate the functions of PS in COVID-19. Here, we connect the data on PS with reference to pulmonary physiology and infection with its possible therapeutic benefit in COVID-19 patients.

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Surfactant Components and Tracheal Aspirate Inflammatory Markers in Preterm Infants with Respiratory Distress Syndrome

Cited by 13 publications

References 36 publications

Tracing exogenous surfactant in vivo in rabbits by the natural variation of 13C

Tracing exogenous surfactant in vivo in rabbits by the natural variation of 13C

Plasma characteristic metabolites of pediatric community‐acquired pneumonia in traditional Chinese medicine syndrome differentiation

The Role of Pulmonary Surfactants in the Treatment of Acute Respiratory Distress Syndrome in COVID-19

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