Surfactant protein-A binds group B Streptococcus enhancing phagocytosis and clearance from lungs of surfactant protein-A-deficient mice
Surfactant protein-A binds group B Streptococcus enhancing phagocytosis and clearance from lungs of surfactant protein-A-deficient mice
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DOI：
10.1165/ajrcmb.20.2.3303
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发表时间：
1999-02-01
影响因子：
6.4
通讯作者：
Korfhagen, TR
中科院分区：
文献类型：
--
作者：
LeVine, AM;Kurak, KE;Korfhagen, TR
表面活性蛋白-A（SP-A）基因靶向小鼠从肺中清除B族链球菌（GBS）的速度比野生型小鼠慢。为了确定SP-A增强GBS的肺清除的机制，在存在和不存在外源性SP-A的情况下，在感染GBS的SP-A（-/-）小鼠中评估SP-A在GES的结合和吞噬中的作用。GBS与外源性SP-A联合给药可降低SP-A（-/-）小鼠肺匀浆中GBS菌落数。SP-A以钙依赖性方式与GBS结合。尽管GBS感染后SP-A（-/-）小鼠与野生型小鼠相比，巨噬细胞的肺浸润没有改变，但SP-A（-/-）小鼠中具有吞噬细菌的肺泡巨噬细胞的数量低于野生型小鼠。当SP-A与GBS共同给药时，吞噬作用显著增加。与野生型对照组相比，感染GBS的SP-A（-/-）小鼠肺泡巨噬细胞产生的氧自由基减少，而在存在外源性SP-A的情况下感染SP-A（-/-）小鼠时，氧自由基增加。SP-A（-/-）小鼠巨噬细胞产生超氧化物（SO）自由基缺乏。SP-A在体内GBS清除中起重要作用，部分通过结合并增强GBS吞噬作用以及通过增加肺泡巨噬细胞的SO产生来介导。
Surfactant protein-A (SP-A) gene-targeted mice clear group B streptococcus (GBS) from the lungs at a slower rate than wild-type mice. To determine mechanisms by which SP-A enhances pulmonary clearance of GBS, the role of SP-A in binding and phagocytosis of GES was assessed in SP-A (-/-) mice infected with GBS in the presence and absence of exogenous SP-A. Coadministration of GBS with exogenous SP-A decreased GBS colony counts in lung homogenates of SP-A (-/-) mice. SP-A bound to GBS in a calcium-dependent manner. Although pulmonary infiltration with macrophages was not altered in SP-A (-/-) versus wild-type mice after GBS infection, the number of alveolar macrophages with phagocytosed bacteria was lower in the SP-A (-/-) mice than in the wild-type mice. When SP-A was coadministered with GBS, phagocytosis was significantly increased. Oxygen radical production by alveolar macrophages from SP-A (-/-) mice infected with GBS was decreased compared with wild-type controls and was in creased when SP-A (-/-) mice were infected in the presence of exogenous SP-A. Superoxide (SO) radical generation was deficient in macrophages from SP-A (-/-) mice. SP-A plays an important role in GBS clearance in vivo, mediated in part by binding to and enhancing GBS phagocytosis and by increasing SO production by alveolar macrophages.