Pikaar J C, Voorhout W F, van Golde L M, Verhoef J, Van Strijp J A, van Iwaarden J F
Eijkman-Winkler Institute for Medical Microbiology, Department of Functional Morphology, Utrecht University, Netherlands.
J Infect Dis. 1995 Aug;172(2):481-9. doi: 10.1093/infdis/172.2.481.
Surfactant proteins A and D (SP-A, SP-D) can interact with lipopolysaccharide (LPS) and stimulate alveolar macrophages. The opsonic activities of SP-A and SP-D for bacteria with different types of LPS and alveolar macrophages were investigated. In flow cytometric studies with fluorescein-labeled rough (J5) and smooth (O111) Escherichia coli and rat alveolar macrophages, SP-A enhanced binding of J5 but not O111 bacteria to macrophages. Most importantly, SP-A enhanced ingestion of J5 bacteria by alveolar macrophages and subsequent bacterial killing. Immunoelectron microscopy demonstrated that J5 bacteria, the interface between the bacterium and the outer membrane of the alveolar macrophage, and ingested bacteria were heavily labeled with SP-A. In contrast, SP-D did not mediate phagocytosis. SP-A acted as an opsonin in the phagocytosis of rough LPS-containing bacteria by alveolar macrophages, emphasizing the possible role for SP-A in the alveolar defense system.
表面活性蛋白A和D(SP-A、SP-D)可与脂多糖(LPS)相互作用并刺激肺泡巨噬细胞。研究了SP-A和SP-D对不同类型LPS细菌及肺泡巨噬细胞的调理活性。在用荧光素标记的粗糙型(J5)和光滑型(O111)大肠杆菌以及大鼠肺泡巨噬细胞进行的流式细胞术研究中,SP-A增强了J5细菌与巨噬细胞的结合,但未增强O111细菌与巨噬细胞的结合。最重要的是,SP-A增强了肺泡巨噬细胞对J5细菌的摄取及随后的细菌杀伤。免疫电子显微镜显示,J5细菌、细菌与肺泡巨噬细胞外膜之间的界面以及被摄取的细菌均被SP-A大量标记。相比之下,SP-D不介导吞噬作用。SP-A在肺泡巨噬细胞对含粗糙LPS细菌的吞噬作用中起调理素作用,强调了SP-A在肺泡防御系统中的可能作用。