Surfactant proteins A and D enhance the phagocytosis of Chlamydia into THP-1 cells
Surfactant proteins A and D enhance the phagocytosis of Chlamydia into THP-1 cells
复制标题
DOI：
10.1152/ajplung.00440.2003
复制
发表时间：
2004-08-01
影响因子：
4.9
通讯作者：
Snyder, JM
中科院分区：
文献类型：
--
作者：
Oberley, RE;Ault, KA;Snyder, JM
衣原体是细胞内细菌病原体，可感染粘膜表面，即肺上皮、生殖道和眼结膜，以及肺泡巨噬细胞。在本研究中，我们发现肺表面活性蛋白A （SP-A）和表面活性蛋白D （SP-D）是参与先天宿主防御的肺聚集物，可增强人单核/巨噬细胞系THP-1细胞对肺炎衣原体和沙眼衣原体的吞噬作用。我们还发现SP-A能够聚集沙眼衣原体和肺炎衣原体，而SP-D只聚集肺炎衣原体。此外，我们发现在SP-A存在下吞噬后，THP-1细胞内48 h的沙眼衣原体活菌数量增加了3.5倍。这些发现表明SP-A和SP-D与衣原体病原体相互作用，增强其吞噬巨噬细胞的能力。此外，在收集物存在下内化的衣原体病原体在吞噬THP-1细胞后能够生长和复制。
Chlamydiae are intracellular bacterial pathogens that infect mucosal surfaces, i.e., the epithelium of the lung, genital tract, and conjunctiva of the eye, as well as alveolar macrophages. In the present study, we show that pulmonary surfactant protein A (SP-A) and surfactant protein D (SP-D), lung collectins involved in innate host defense, enhance the phagocytosis of Chlamydia pneumoniae and Chlamydia trachomatis by THP-1 cells, a human monocyte/macrophage cell line. We also show that SP-A is able to aggregate both C. trachomatis and C. pneumoniae but that SP-D only aggregates C. pneumoniae. In addition, we found that after phagocytosis in the presence of SP-A, the number of viable C. trachomatis pathogens in the THP-1 cells 48 h later was increased similar to3.5-fold. These findings suggest that SP-A and SP-D interact with chlamydial pathogens and enhance their phagocytosis into macrophages. In addition, the chlamydial pathogens internalized in the presence of collectins are able to grow and replicate in the THP-1 cells after phagocytosis.