Hirose K, Ezaki T, Miyake M, Li T, Khan A Q, Kawamura Y, Yokoyama H, Takami T
Department of Microbiology, Gifu University, School of Medicine, Japan.
FEMS Microbiol Lett. 1997 Feb 15;147(2):259-65. doi: 10.1111/j.1574-6968.1997.tb10251.x.
We examined the intracellular survival of Vi-capsulated (lipopolysaccharide; (LPS)-masked) and Vi-deleted (LPS-exposed) Salmonella typhi strains inside macrophage cell lines. Growth of LPS-exposed S. typhi was inhibited in both mouse and human macrophage cell lines. However, the LPS-exposed strain survived in a CD14-deficient mouse macrophage cell lines. Wild-type S. typhi strain, which expressed the Vi antigen and masked LPS, survived in the resting human macrophage cell line. When the Vi-capsulated S. typhi entered the cells, the production of tumor necrosis factor-alpha (TNF-alpha) was suppressed. In contrast, S. typhimurium and LPS-exposed S. typhi stimulated the macrophages to produce a high level of TNF-alpha.
我们检测了有Vi荚膜（脂多糖；（LPS）被掩盖）和缺失Vi（LPS暴露）的伤寒沙门氏菌菌株在巨噬细胞系内的细胞内存活情况。LPS暴露的伤寒沙门氏菌在小鼠和人巨噬细胞系中的生长均受到抑制。然而，LPS暴露菌株能在CD14缺陷的小鼠巨噬细胞系中存活。表达Vi抗原并掩盖LPS的野生型伤寒沙门氏菌菌株能在静息的人巨噬细胞系中存活。当有Vi荚膜的伤寒沙门氏菌进入细胞时，肿瘤坏死因子-α（TNF-α）的产生受到抑制。相比之下，鼠伤寒沙门氏菌和LPS暴露的伤寒沙门氏菌刺激巨噬细胞产生高水平的TNF-α。
