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发的篇幅的确比较长，但希望各位虫友能够帮帮忙 声明请您不要拿灵格斯或google翻译的东西给我 提前谢谢好心的人 SP-D. SP-D is a hydrophilic 43 kDa collectin belonging to the superfamily of collagen containing C-type lectins, and is structurally similar to SP-A. Produced in Type II alveolar cells, it is also found in epithelial cells and secretory glands of the gastrointestinal tract. SP-D plays an important role in the innate immune system by binding to specific carbohydrate and lipid structures on the surface of bacteria, viral particles, fungi and protozoa through a calciumdependent interaction . It has also been thought to have a role in the control of lung inflammation . The SP-D gene consists of 8 exons spanning >11 kb of DNA located on the long arm of human chromosome 10 . Levels of SP-D and SP-A are potential markers for lung maturation because studies of amniotic fluid and lung tissue have demonstrated increasing levels of SP-D with increasing gestational age . Transcription of SP-D is regulated by direct interaction of nuclear factor of activated T cells (NFAT) with TTF-1 . Metabolism of surfactant Overview of surfactant metabolism Pulmonary surfactant is synthesized, assembled, transported and secreted into the alveolus where it is degraded. It is then recycled in a highly complex and regulated mechanism. This process is slower in newborns (especially those born prematurely) than in adults or those with lung injury. The rate of synthesis and the half-life of surfactant are influenced by many factors. Surfactant synthesis and turnover in preterm infants using stable isotopes of glucose, acetate and palmitic acid demonstrates that synthesis from glucose to surfactant phosphatidylcholine (PC) takes approximately 19 h and reaches a peak at 70 h after labeling. The absolute production rate of PC is 4.2 mg/kg/day while the half-life is 113 (±25) hours . The fractional synthesis rate of surfactant PC from plasma palmitate was significantly higher than that from palmitate synthesized de novo from acetate or glucose, but only accounted for half of the total surfactant production in preterm infants . Surfactant secretion can be stimulated by a number of mechanisms. Type II cells have beta-adrenergic receptors and respond to beta-agonists with increased surfactant secretion . Purines, such as adenosine triphosphate are potent stimulators of surfactant secretion and may be important for its secretion at birth. Mechanical stretch such as lung distension and hyperventilation, have also been found to be involved in stimulating surfactant secretion. Stretch-mediated enhancement of surfactant secretionduring exercise prevents a loss of alveolar surfactant . Hormones also play a role in surfactant secretion. Thyroxine accelerates Type II cell differentiation while acting synergistically with glucocorticoids to enhance the distensibility of the lung and DPPC synthesis. However, glucocorticoids alone are used in clinical practice to induce lung maturity because studies have not shown that the synergistic effect with thyroxine is greater than the effect achieved by glucocorticoids alone . Type II cells, macrophages and the alveolar lining play a major role in surfactant turnover. Cyclical changes in the alveolar surface appear to promote conversion of newly secreted, apoprotein-rich, active surfactant aggregates into protein-poor, inactive forms that are ready for clearance . Surfactant components are removed from air spaces through uptake by Type II cells and alveolar macrophages, with the bulk done by the Type II cells. The phospholipids are taken up by endocytosis into the Type II cells where they are recycled and re-secreted, whereas the SPs are recycled back into the lamellar bodies for re-secretion with surfactant. Surfactant is also transformed during the cyclic compression and expansion of alveoli from large, highly surface-active aggregates into smaller, less active subtypes . Defects in surfactant metabolism Defective surfactant metabolism leads to both morbidity and mortality in preterm and term neonates. In general, defects in surfactant metabolism occur due to accelerated breakdown of the surfactant complex by oxidation, proteolytic degradation, and inhibition . Some inherited surfactant gene defects have also been implicated. Respiratory distress syndrome. Respiratory distress syndrome (RDS) is one of the most common causes of morbidity in preterm neonates. It occurs worldwide with a slight male predominance . Patients present shortly after birth with apnea, cyanosis, grunting, inspiratory stridor, nasal flaring, poor feeding and tachypnea. There may also be intercostal or subcostal retractions. Radiological findings include a diffuse reticulogranular ‘‘ground glass” appearance (resulting from alveolar atelectasis) with superimposed air bronchograms . The preterm infant who has RDS has low amounts of surfactant that contains a lower percent of disaturated phosphatidylcholine species, less phosphatidylglycerol, and less of all the surfactant proteins than surfactant from a mature lung. Minimal surface tensions are also higher for surfactant from preterm than term infants . The diagnosis can be confirmed by biochemical evidence of surfactant deficiency or pathologically. Lungs of infants who have died from RDS show alveolar atelectasis, alveolar and interstitial edema and diffuse hyaline membranes in distorted small airways . Prenatal corticosteroids and postnatal surfactant replacement therapy significantly reduce the incidence, severity and mortality associated with RDS, and surfactant therapy has become the standard of care in management of preterm infants with RDS . Meconium aspiration syndrome. Meconium aspiration syndrome (MAS) is an important cause of morbidity and mortality from respiratory distress in the perinatal period and affects an estimated 25,000 neonates in the United States each year . Meconium staining of the amniotic fluid or fetus is an indication of fetal distress. Fetal respiration is associated with movement of fluid from the airways out into the amniotic fluid. However, in the presence of fetal distress, gasping may be initiated in utero leading to aspiration of amniotic fluid and its contents, which includes meconium, into the large airways . Acute lung injury is characterized by airway obstruction, pneumonitis, pulmonary hypertension, ventilation/perfusion mismatch, acidosis and hypoxemia.The mechanisms underlying surfactant inactivation by meconium are not fully understood, but it has been shown that meconium destroys the fibrillary structure of surfactant and decreases its surface adsorption rate [50]. MAS is associated with an inflammatory response characterized by the presence of elevated cell count and pro-inflammatory cytokines IL-1b, IL-6 and IL-8 as early as in the first 6 h and significantly decreased by 96 h of life [49]. Phospholipase-A2, (PLA2) present in meconium, has been found to inhibit the activity of surfactant in vitro in a dose-dependent manner, through the competitive displacement of surfactant from the alveolar film [51]. PLA2 is also known to induce hydrolysis of DPPC, releasing free fatty acids and lyso-PC which damage the alveolar–capillary membrane and induce intrapulmonary sequestration of neutrophils [52]. Exogenous surfactant replacement either as bolus therapy or with a diluted surfactant lung lavage have been shown to reverse the hypoxemia and reduce pneumothoraces caused by meconium aspiration, decrease requirement for extracorporeal membrane oxygenation (ECMO), decrease duration of oxygen therapy and mechanical ventilation, and reduce the duration of hospital stays [47,53]. A comparison of various surfactant treatment regimens in MAS did not find the superiority of one form of therapy over another, and may be related to the heterogeneous nature of this form of lung injury [54]. In an underpowered randomized trial comparing bolus (N = 6) versus surfactant lavage (N = 7) followed by inhaled nitric oxide, infants receiving surfactant lavage has significant improvements in oxygenation, decreases in mean airway pressure, and arterial-alveolar oxygen tension gradients; however there were no significant differences in duration of assisted ventilation, nitric oxide therapy, or hospitalization[55]. Pulmonary hemorrhage. Pulmonary hemorrhage may also be associated with respiratory distress syndrome (RDS) and can be difficult to differentiate from it by radiography [46]. It occurs subsequent to a rise in lung capillary pressure due to the effects of hypoxia, volume overload, congestive heart failure, or it may be induced by trauma from mechanical suctioning of the newborn airway. There is a strong association between significant left to right ductal shunting and pulmonary hemorrhage in preterm babies [45,56]. There is a build up of the capillary filtrate in the interstitial space which can then burst through into the airspaces through the pulmonary epithelium. Neutrophils are released following endothelial damage and they, in turn, express proteases, oxygen free-radicals and cytokines. These free oxygen molecules damage the Type II cells that produce SPs, thus inhibiting production of the proteins. Elastase, one of these proteases, damages and degrades SP-A, thereby inhibiting SP-A mediated surfactant lipid aggregation and adsorption in vitro [2]. Pulmonary hemorrhage is also considered a rare adverse event associated with surfactant replacement therapy [45,46]. Acute respiratory distress syndrome. Acute respiratory distress syndrome (ARDS) is a significant cause of morbidity and mortality in all age groups following sepsis, hemorrhage, or other forms of lung injury. It is defined as a severe form of acute lung injury (ALI) and a syndrome of acute pulmonary inflammation. ALI/ARDS is characterized by sudden onset, impaired gas exchange, decreased static compliance, and by a non-hydrostatic pulmonary edema [57]. Infection is the most common cause of development of ARDS in children [58]. The lungs appear particularly vulnerable in the first year of life. Premature neonates with chronic lung disease who develop viral pneumonia, older children with immune deficiency syndromes, and those with childhood malignancies are especially at risk [58]. The hallmark in the pathophysiology of the acute event is an increase in the permeability of the alveolar–capillary barrier as a result of injury to the endothelium and/or alveolar lining cells. Damage to the alveolar Type I cells leads to an influx of proteinrich edema-fluid into the alveoli, as well as decreased fluid clearance from the alveolar space. Neutrophils are attracted into the airways by host bacterial and chemotactic factors and express enzymes and cytokines which further damage the alveolar epithelial cells [2]. Type II epithelial cell injury leads to a decrease in surfactant production, with resultant alveolar collapse. Four clinical criteria must be met to establish a clinical diagnosis of ARDS: (i) acute disease onset, (ii) bilateral pulmonary infiltrates on chest radiograph, (iii) pulmonary capillary wedge pressure <18 mmHg or absence of clinical evidence of left atrial hypertension and (iv), ratio between arterial oxygen partial pressure (PaO2) and the fraction of inspired oxygen (FiO2) <200 [57]. In contrast, patients that meet the first three criteria, but exhibit a PaO2/FiO2 ratio between 200 and 300, are defined as having ALI. Despite the introduction of novel treatments, the mortality from ARDS in the pediatric age group still remains high. Attempts to treat ARDS with an SP-C surfactant, Venticute (Altana Pharma, Germany), were ineffective [59]. However, the use of calfactant (Infasurf) in younger children with ALI was effective in reducing ventilator days and increasing survival [60]. Pulmonary alveolar proteinosis. Pulmonary alveolar proteinosis (PAP) is a rare lung disease in which the alveoli fill with PL-rich proteinaceous material. This substance stains for periodic acid- Schiff and is nearly identical to surfactant [61]. PAP occurs in three clinically distinct forms; congenital, secondary and acquired. Congenital PAP is an uncommon cause of respiratory failure in fullterm newborns known to be caused by inborn errors of surfactant protein metabolism . Lysinuric protein intolerance has also been implicated as a secondary cause of congenital/infantile PAP. Although the specific cellular pathogenesis is unknown, recent observations in genetically altered mice have led to the speculation that either absolute deficiency of alveolar cells or hyporesponsiveness of the alveolar cells to granulocyte-macrophage colony stimulating factor (GM-CSF) is etiologic to PAP . However, the role of GM-CSF in congenital PAP is not clear as antibodies against GM-CSF have not been identified in infants with this condition. The standard of care is the use of whole lung lavage to relieve the symptoms . The prognosis for infants with congenital PAP has been uniformly poor and they die within the first year of life, despite maximal medical therapy . However, a recent report also showed successful treatment of congenital PAP with monthly doses of intravenous Immunoglobulin with the patient remaining free of respiratory symptoms for more than 3 years . |
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