Linke M J, Harris C E, Korfhagen T R, McCormack F X, Ashbaugh A D, Steele P, Whitsett J A, Walzer P D
Research Service, Department of Veterans Affairs Medical Center, and Divisions of Infectious Diseases and Pulmonary/Critical Care Medicine, University of Cincinnati, Cincinnati, OH 45220, USA.
J Infect Dis. 2001 Mar 15;183(6):943-52. doi: 10.1086/319252. Epub 2001 Feb 15.
Immunosuppressed Swiss Black mice deficient in surfactant protein A (SP-A(-/-)) and wild-type control mice (SP-A(+/+)) were exposed to Pneumocystis carinii by environmental exposure, intratracheal inoculation, and direct exposure to other infected animals. The frequency and intensity of P. carinii infection were significantly greater in the SP-A(-/-) mice by all 3 methods of exposure. P. carinii free of SP-A and alveolar macrophages were isolated from SP-A(-/-) mice and were tested in an in vitro attachment assay. Pretreatment of P. carinii with human SP-A resulted in a significant dose-dependent increase of the adherence of P. carinii to the macrophages. Thus, SP-A plays a role in host defense against P. carinii in vivo, perhaps by functioning as a nonimmune opsonin.
通过环境暴露、气管内接种以及直接接触其他受感染动物，将缺乏表面活性蛋白A（SP-A(-/-)）的免疫抑制瑞士黑小鼠和野生型对照小鼠（SP-A(+/+)）暴露于卡氏肺孢子虫。通过所有3种暴露方法，SP-A(-/-)小鼠中卡氏肺孢子虫感染的频率和强度显著更高。从SP-A(-/-)小鼠中分离出不含SP-A的卡氏肺孢子虫和肺泡巨噬细胞，并在体外黏附试验中进行测试。用人SP-A预处理卡氏肺孢子虫导致卡氏肺孢子虫对巨噬细胞的黏附显著剂量依赖性增加。因此，SP-A在体内宿主抵御卡氏肺孢子虫的防御中发挥作用，可能是作为一种非免疫调理素发挥作用。
