Surfactant therapy of newborn rabbits impairs lung macrophage bactericidal activity.

Surfactant therapy of newborn rabbits impairs lung macrophage bactericidal activity.
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新生兔的表面活性剂治疗会损害肺巨噬细胞的杀菌活性。

DOI:
10.1152/jappl.1988.65.1.137
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发表时间:
1988
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Barrett,CT
Barrett,CT
中科院分区:
--
文献类型:
--
作者:
Sherman,MP;D'Ambola,JB;Aeberhard,EE;Barrett,CT

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由于体外研究表明充满磷脂囊泡的肺泡巨噬细胞(PAM)具有抑制的杀微生物能力,因此我们测试了表面活性剂处理后新生PAM的肺内杀菌活性。足月新生兔气管内接受同种表面活性剂或两种人工磷脂囊泡制剂之一,然后用B组链球菌(GBS)进行肺部气溶胶感染。肺部感染后4小时,与未处理动物或接受肺内注射表面活性剂载体的动物相比,用同源表面活性剂和一种人工表面活性剂处理的动物中GBS的吞噬细胞杀伤减少70-90%(P小于0.02)。与对照组相比,另一种人工磷脂制剂使肺内GBS失活减少30-40%。三种制剂中的磷脂囊泡被新生PAM贪婪地摄取和加工。GBS的体内杀伤作用的减弱并不归因于PAM对GBS的活力或吞噬行为的降低。在新生PAM中明显的杀菌缺陷似乎与制剂中大磷脂囊泡的摄取有关,而不是与表面活性剂本身的磷脂含量有关。当在体外条件下,刺激肺泡环境中使用,天然表面活性剂制剂促进GBS增殖,而人工制剂没有。我们的研究结果表明,表面活性剂给药会降低新生儿PAM的杀菌活性。我们的结论是,需要进一步的调查,以确定肺表面活性物质替代治疗的效果失去防御。
Because in vitro studies indicate that pulmonary alveolar macrophages (PAM's) filled with phospholipid vesicles have depressed microbicidal capacity, we tested the intrapulmonary bactericidal activity of newborn PAM's after surfactant treatment. Term newborn rabbits received intratracheally either homologous surfactant or one of two artificial phospholipid vesicle preparations followed by pulmonary aerosol infection with group B streptococci (GBS). Four hours after lung infection, phagocytic killing of GBS was reduced by 70-90% in animals treated with the homologous and one of the artificial surfactants compared with untreated animals or animals that received intrapulmonary injections of the surfactant vehicle (P less than 0.02). The other artificial phospholipid preparation decreased intrapulmonary inactivation of GBS by 30-40% compared with the controls. The phospholipid vesicles in the three preparations were avidly ingested and processed by newborn PAM's. The diminished in vivo killing of GBS was not attributed to decreased viability or phagocytic behavior of the PAM's toward GBS. The bactericidal defect that was evident in the newborn PAM's appeared related to the uptake of large phospholipid vesicles in the preparations rather than to the phospholipid content of the surfactants themselves. When in vitro conditions that stimulated the alveolar environment were used, the natural surfactant preparation promoted GBS proliferation, whereas the artificial preparations did not. Our findings indicate that surfactant administration reduces the bactericidal activity of neonatal PAM's. We conclude that additional investigations are needed to ascertain the effect of surfactant replacement therapy on lost defenses of the lung.