Surfactant protein A-deficient mice are susceptible to group B streptococcal infection.
Surfactant protein A-deficient mice are susceptible to group B streptococcal infection.
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DOI：
10.4049/jimmunol.158.9.4336
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发表时间：
1997-05
影响因子：
4.4
通讯作者：
A. Levine;M. Bruno;K. Huelsman;G. Ross;J. Whitsett;T. Korfhagen
中科院分区：
文献类型：
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作者：
A. Levine;M. Bruno;K. Huelsman;G. Ross;J. Whitsett;T. Korfhagen
为了确定表面活性蛋白A（SP-A）在宿主防御中的作用，通过同源重组靶向小鼠SP-A位点以产生缺乏SP-A的小鼠。用B组链球菌（GBS）经阴道滴注感染SP-A -/-和对照小鼠。肺浸润6和24小时后感染SP-A -/-比对照组小鼠更严重，并与肺匀浆中GBS数量增加有关。在SP-A -/-小鼠中更频繁地观察到GBS向脾脏的传播。两组中巨噬细胞的肺浸润相似;然而，SP-A缺陷小鼠中与肺泡巨噬细胞相关的细菌数量减少。在GBS滴注后，表面活性蛋白D（另一种已知的肺聚集素）没有可检测到的代偿性增加。SP-A在体内发挥重要作用，增强GBS从肺中的清除并抑制生物体的全身传播。
To determine the role of surfactant protein A (SP-A) in host defense, the murine SP-A locus was targeted by homologous recombination to produce mice lacking SP-A. SP-A -/- and control mice were infected with group B streptococcus (GBS) by intratracheal instillation. Pulmonary infiltration 6 and 24 h following infection was more severe in SP-A -/- than in control mice, and was associated with increased numbers of GBS in lung homogenates. Dissemination of GBS to the spleen was observed more frequently in SP-A -/- mice. Pulmonary infiltration with macrophages was similar in both groups; however, the number of bacteria associated with alveolar macrophages was decreased in the SP-A-deficient mice. There was no detectable compensatory increase in surfactant protein D, the other known pulmonary collectin, in response to GBS instillation. SP-A plays an important role in vivo, enhancing clearance of GBS from the lung and inhibiting systemic dissemination of the organism.