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首页> 外文期刊>American Journal of Physiology >Surfactant protein A regulates surfactant phospholipid clearance after LPS-induced injury in vivo.
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Surfactant protein A regulates surfactant phospholipid clearance after LPS-induced injury in vivo.

机译：表面活性剂蛋白A调节LPS诱导的体内损伤后表面活性剂磷脂的清除。

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摘要

Previous in vitro studies have suggested that surfactant protein A (SP-A) may play a role in pulmonary surfactant homeostasis by mediating surfactant secretion and clearance. However, mice made deficient in SP-A [SP-A (-/-) animals] have relatively normal levels of surfactant compared with wild-type SP-A (+/+) animals. We hypothesize that SP-A may play a role in surfactant homeostasis after acute lung injury. Bacterial lipopolysaccharide was instilled into the lungs of SP-A (-/-) mice and SP-A (+/+) mice to induce injury. Surfactant phospholipid levels were increased 1.6-fold in injured SP-A (-/-) animals, although injury did not alter [3H]choline or [14C]palmitate incorporation into dipalmitoylphosphatidylcholine (DPPC), suggesting no change in surfactant synthesis/secretion 12 h after injury. Clearance of [3H]DPPC from the lungs of injured SP-A (-/-) animals was decreased by approximately 40%. Instillation of 50 microg of exogenous SP-A rescued both the clearance defect and the increased phospholipiddefect in injured SP-A (-/-) animals, suggesting that SP-A may play a role in regulating clearance of surfactant phospholipids after acute lung injury.
机译：先前的体外研究表明，表面活性剂蛋白A（SP-A）可能通过介导表面活性剂的分泌和清除而在肺表面活性剂稳态中发挥作用。但是，与野生型SP-A（+ / +）动物相比，SP-A缺陷的小鼠[SP-A（-/-）动物]的表面活性剂水平相对正常。我们假设SP-A可能在急性肺损伤后在表面活性剂稳态中起作用。将细菌脂多糖滴入SP-A（-/-）小鼠和SP-A（+ / +）小鼠的肺中以诱导损伤。尽管受伤并未改变[3H]胆碱或[14C]棕榈酸酯掺入二棕榈酰磷脂酰胆碱（DPPC）中，但表面活性剂磷脂水平在受伤的SP-A（-/-）动物中增加了1.6倍，表明表面活性剂合成/分泌没有变化12受伤后h。从受伤的SP-A（-/-）动物的肺中清除[3H] DPPC的清除率降低了大约40％。在受伤的SP-A（-/-）动物中滴注50微克外源SP-A可以挽救清除缺陷和增加的磷脂缺陷，这表明SP-A可能在急性肺损伤后在调节表面活性剂磷脂的清除中发挥作用。

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