The Importance of Surfactant on the Development of Neonatal Pulmonary Diseases

Lyra, Priscila Pinheiro Ribeiro; Diniz, Edna Maria de Albuquerque

doi:10.1590/s1807-59322007000200014

Cited by 15 publications

(11 citation statements)

References 61 publications

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“…Similarly, decreased serum level of SP-B protein, caused by a hereditary deficiency in the SP-B gene, frequently results in unexplained respiratory distress in infants due to defective surfactant maturation [34,50]. The inability to produce multiple SPs due to autosomal recessive genetic alterations causes fatal respiratory insufficiency, indicating the fundamental role of SPs in normal pulmonary function [51]. Hallman et al demonstrated that a major SP-A haplotype, interacting with SP-B Ile131Thr polymorphism and other environmental risk factors, increased the risk of RDS [52].…”

Section: Discussionmentioning

confidence: 99%

Genetic Polymorphisms of SP-A, SP-B, and SP-D and Risk of Respiratory Distress Syndrome in Preterm Neonates

Chang¹,

Li²,

Li³

et al. 2016

Med Sci Monit

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BackgroundWe examined selected polymorphisms in 3 pulmonary surfactant-associated proteins (SP) for their influence on serum SP levels and risk of respiratory distress syndrome (RDS) in preterm neonates.Material/MethodsPremature infants from a Han population were enrolled, including 100 premature infants with RDS (case group) and 120 premature infants without RDS (control group). SNP genotyping for SP-A (+186A/G and +655C/T), SP-B (−18A/C and 1580C/T), and SP-D (Met11ThrT/C and Ala160ThrG/A) used polymerase chain reaction-restriction fragment length polymorphism. Haplotypes were calculated with Shesis software and serum SP-A/B/D levels were quantified by ELISA.ResultsCase and control groups exhibited significant differences in genotype and allele frequencies of SP-A (+186A/G, +655C/T) and SP-B (1580C/T). However, no statistically significant differences were observed in the allele and genotype frequencies of SP-B −18A/C, SP-D Met11ThrT/C, and SP-D Ala160ThrG/A. Importantly, serum SP-A and SP-B levels were reduced in RDS patients carrying SP-A (+186A/G, +655C/T) and SP-B (1580C/T) polymorphisms. AA genotype of +186A/G, SP-A level, and CC genotype of 1580C/T were independently correlated with increased RDS risk.ConclusionsSP-A (+186A/G) and SP-B (1580C/T) polymorphisms are strongly associated with the risk of RDS in preterm infants. Notably, reduced serum SP-A levels were correlated with a high risk of RDS and may serve as novel biomarkers for RDS detection and monitoring.

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Section: Discussionmentioning

confidence: 99%

Genetic Polymorphisms of SP-A, SP-B, and SP-D and Risk of Respiratory Distress Syndrome in Preterm Neonates

Chang¹,

Li²,

Li³

et al. 2016

Med Sci Monit

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“…In neonates, deficiency of surfactant protein production or secretion due to pulmonary immaturity can cause clinical disorders, such as respiratory distress syndrome or bronchopulmonary dysplasia. Respiratory distress syndrome is a major cause of high morbidity and mortality in premature infants [8], [9], [10].…”

Section: Introductionmentioning

confidence: 99%

Disruption of Sorting Nexin 5 Causes Respiratory Failure Associated with Undifferentiated Alveolar Epithelial Type I Cells in Mice

Jeong

et al. 2013

PLoS ONE

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Sorting nexin 5 (Snx5) has been posited to regulate the degradation of epidermal growth factor receptor and the retrograde trafficking of cation-independent mannose 6-phosphate receptor/insulin-like growth factor II receptor. Snx5 has also been suggested to interact with Mind bomb-1, an E3 ubiquitin ligase that regulates the activation of Notch signaling. However, the in vivo functions of Snx5 are largely unknown. Here, we report that disruption of the Snx5 gene in mice (Snx5-/- mice) resulted in partial perinatal lethality; 40% of Snx5-/- mice died shortly after birth due to cyanosis, reduced air space in the lungs, and respiratory failure. Histological analysis revealed that Snx5-/- mice exhibited thickened alveolar walls associated with undifferentiated alveolar epithelial type I cells. In contrast, alveolar epithelial type II cells were intact, exhibiting normal surfactant synthesis and secretion. Although the expression levels of surfactant proteins and saturated phosphatidylcholine in the lungs of Snx5-/- mice were comparable to those of Snx5+/+ mice, the expression levels of T1α, Aqp5, and Rage, markers for distal alveolar epithelial type I cells, were significantly decreased in Snx5 -/- mice. These results demonstrate that Snx5 is necessary for the differentiation of alveolar epithelial type I cells, which may underlie the adaptation to air breathing at birth.

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“…New research on the differences between the allelic variants of the surfactant protein genes is leading to the understanding of individual susceptibility to the development of pulmonary diseases in the neonates. 30 Randomised controlled trials to evaluate the efficacy of combining prophylactic surfactant and early nasal continuous positive airway pressure in preterm infants 31,32 also need to be done in our country to evaluate and establish the most effective and safest interventions for preterm neonates at risk of developing RDS and associated morbidities. …”

Section: Discussionmentioning

confidence: 99%

Role of prophylactic surfactant in preterm infants

Singh¹,

Rana²,

Mathai

2011

Medical Journal Armed Forces India

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INTRODUCTIONRespiratory distress syndrome (RDS) in preterm neonates is caused by a deficiency or dysfunction of pulmonary surfactant. Surfactant lines the alveolar surface and prevents atelectasis at end expiration. Pulmonary surfactant is predominantly dipalmitoylphosphatidylcholine with lesser amounts of other phospholipids including phosphatidylglycerol, phosphatidylethanolamine, and phosphatidylinositol. Pulmonary surfactant also contains neutral lipids and distinct surfactant proteins. The physiologic function of surfactant includes the ability to lower surface tension, as well as the ability to rapidly adsorb and spread, associated with the respiratory cycle. The first attempts to utilise synthetic surfactants occurred in the 1960s. The first successful animal model of surfactant replacement therapy was conducted by Enhorning and coworkers in 1972. Enhorning administered a crude natural surfactant extract obtained from lavage of the lungs of mature rabbits 1 directly into the trachea of immature rabbits. Improvement in lung compliance and alveolar expansion was noted. Success in animal models led to widespread clinical trials of surfactant therapy in the human newborns. A systematic review of the seven randomised controlled trials that compare the prophylactic administration of synthetic surfactant to control treatment in preterm infants at risk of developing RDS suggests that prophylactic administration of synthetic surfactant leads to a significant decrease in the risk of pneumothorax, pulmonary interstitial emphysema, and neonatal mortality.2-4 So far, no trials of prophylactic surfactant in preterm neonates were carried out in our country because of the prohibitive cost of the imported drug. During the last decade, preparations of exogenous surfactant have been marketed in our country. This has made it possible to evaluate the prophylactic role of surfactant in preventing respiratory distress syndrome and its associated morbidities in preterm neonates. The present study was designed to find out whether prophylactic administration of surfactant leads to a significant decrease in the risk of neonatal mortality and neonatal morbidity. MATERIALS AND METHODSThis was an experimental study in which a total of 125 preterm newborns less than 34 weeks gestation were studied. The study was carried out in two phases from December 2003 to November 2006. The inclusion criteria were designed to include newborn babies who were less than 34 weeks gestational age at the time of birth. The gestational age assessment was Role of prophylactic surfactant in preterm infants

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The Importance of Surfactant on the Development of Neonatal Pulmonary Diseases

Cited by 15 publications

References 61 publications

Genetic Polymorphisms of SP-A, SP-B, and SP-D and Risk of Respiratory Distress Syndrome in Preterm Neonates

Genetic Polymorphisms of SP-A, SP-B, and SP-D and Risk of Respiratory Distress Syndrome in Preterm Neonates

Disruption of Sorting Nexin 5 Causes Respiratory Failure Associated with Undifferentiated Alveolar Epithelial Type I Cells in Mice

Role of prophylactic surfactant in preterm infants

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