The role of surfactant treatment in preterm infants and term newborns with acute respiratory distress syndrome

Wirbelauer, Johannes; Speer, Christian P.

doi:10.1038/jp.2009.30

Cited by 42 publications

(28 citation statements)

References 45 publications

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“…Due to its success in the treatment of premature infants with respiratory distress syndrome, surfactant replacement therapy is under investigation as a potential therapy for ALI/ARDS in pediatric and adult patients (23,24). Initial studies using surfactant have not been encouraging; however, these studies used an aerosolized form of surfactant or protein-free phospholipid preparations of surfactant that did not contain SP-D (25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

Surfactant Protein D Deficiency Increases Lung Injury during Endotoxemia

King

Kingma²

2011

Am J Respir Cell Mol Biol

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Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), are major causes of acute respiratory failure with high rates of morbidity and mortality. Although surfactant protein (SP)-D plays a critical role in pulmonary innate immunity and several clinical studies suggest that this protein may be implicated in the pathophysiology of ARDS, little is known regarding the function of SP-D in ARDS. In the present study, we induced indirect lung injury by intraperitoneal injection of LPS and direct lung injury by intratracheal injection of LPS in wild-type and Sftpd 2/2 mice to elucidate the role of SP-D during ALI/ARDS. Results indicate that pulmonary levels of IL-6 and TNF-a were higher in Sftpd 2/2 mice when compared with wild-type mice. However, the magnitude of this difference was 10-fold greater after indirect lung injury compared with direct lung injury. After indirect lung injury, there was a 2-fold increase in the number of pulmonary monocyte/macrophages in the Sftpd 2/2 mice when compared with wild-type mice, whereas pulmonary neutrophils were not increased. After indirect injury, the concentration of granulocyte-macrophage colony stimulating factor (GM-CSF) was approximately 5-fold greater in Sftpd 2/2 mice than wild-type mice. In contrast, after direct injury, the concentration of GM-CSF was 20-fold less in Sftpd 2/2 mice than wild-type mice. Despite increased inflammatory cells and markers of inflammation, survival in Sftpd 2/2 mice after indirect lung injury was paradoxically increased. In conclusion, these results suggest that SP-D inhibits pulmonary inflammation and migration of peripheral monocyte/macrophages into the lung through GM-CSF-dependent pathways during indirect lung injury.Keywords: surfactant protein D; acute respiratory distress syndrome; macrophage; GM-CSF Acute lung injury (ALI), and its severe form, acute respiratory distress syndrome (ARDS), are characterized by acute pulmonary inflammation and pulmonary edema. The inflammatory response in ARDS originates from the loss of vascular endothelial cell integrity, resulting in alveolar capillary leak, development of protein-rich pulmonary edema, surfactant dysfunction, pulmonary inflammation, damage to the lung parenchyma and pulmonary epithelium, and respiratory insufficiency (1). The outcome of this self-perpetuating process is excessive lung injury and, in many cases, multiple organ dysfunction syndrome, organ failure, and death.ALI/ARDS develops from a variety of clinical disorders that can be differentiated into those associated with direct lung injury (e.g., pneumonia, aspiration) and those causing indirect lung injury (e.g., sepsis, shock). Although the resulting pulmonary inflammation and damage to the lung parenchyma are similar, there is a growing body of evidence that suggests that the two modes of injury have unique underlying pathophysiological mechanisms (2).Analysis of bronchoalveolar lavage fluid (BALF) samples from adult patients with ARDS has demonstrated that, in addition to inflammation, alte...

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Section: Discussionmentioning

confidence: 99%

Surfactant Protein D Deficiency Increases Lung Injury during Endotoxemia

King

Kingma²

2011

Am J Respir Cell Mol Biol

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“…Protein leakage into the alveoli and airways of preterm infants takes place within 1 h after initiation of mechanical ventilation [51,81] . At a postnatal age of 10-14 days, preterm infants who later developed BPD had a large increase of albumin concentrations in their airway secretions; albumin and other serum proteins profoundly contribute to alveolar edema, to the inactivation of the surfactant system and a deterioration of lung function [44,82] . Magnetic resonance imaging in infants with BPD showed an increased lung water content and a gravity-induced collapse of the lung [83] .…”

Section: Increased Alveolar Capillary Permeabilitymentioning

confidence: 99%

Chorioamnionitis, Postnatal Factors and Proinflammatory Response in the Pathogenetic Sequence of Bronchopulmonary Dysplasia

Speer¹

2009

Neonatology

177

139

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Pulmonary inflammation has a central role in the multifactorial and complex pathogenesis of bronchopulmonary dysplasia. Pre- and postnatal factors such as chorioamnionitis, oxygen toxicity, mechanical ventilation and postnatal infections can induce and perpetuate an injurious and complex inflammatory response in the airways and lung tissue of very immature infants. This inflammatory process is characterized by the accumulation of inflammatory cells and an arsenal of proinflammatory mediators such as cytokines, toxic oxygen radicals, lipid mediators and potent proteases. An imbalance between pro- and anti-inflammatory factors favoring the proinflammatory process can be considered as a hallmark of lung injury. In addition, impaired mechanisms of tissue remodeling and repair together with a subnormal generation of growth factors could affect alveolarization and vascular development with lifelong consequences for the infants with bronchopulmonary dysplasia.

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“…Exogenous surfactant is also used for newborns and babies, as ARDS involves secondary deficiency of the natural surfactant, which results in lung collapse. (17) In the last 10 years, the use of exogenous surfactant in the treatment of respiratory disorder of newborns has significantly reduced the mortality of premature babies; nevertheless, it remains the main cause of death of such infants. Respiratory distress suffered by a newborn, results from two pathophysiological mechanisms: surfactant deficiency and action of surfactant inhibitors.…”

Section: Ards Pathophysiologymentioning

confidence: 99%

“…They have low functional residual capacity and insufficient amount of surfactant. (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) …”

Section: Ards Pathophysiologymentioning

confidence: 99%

Exogenous Surfactant Treatment in Children with ARDS

2013

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The role of surfactant treatment in preterm infants and term newborns with acute respiratory distress syndrome

Cited by 42 publications

References 45 publications

Surfactant Protein D Deficiency Increases Lung Injury during Endotoxemia

Surfactant Protein D Deficiency Increases Lung Injury during Endotoxemia

Chorioamnionitis, Postnatal Factors and Proinflammatory Response in the Pathogenetic Sequence of Bronchopulmonary Dysplasia

Exogenous Surfactant Treatment in Children with ARDS

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