Ishibashi Y, Arai T
Department of Microbiology, Meiji College of Pharmacy, Tokyo, Japan.
FEMS Microbiol Immunol. 1990 May;2(1):35-43. doi: 10.1111/j.1574-6968.1990.tb03476.x.
Phagosome-lysosome fusion in murine macrophages infected with S. typhimurium LT2 or S. typhi 1079 was investigated. Fusion of phagosome containing S. typhimurium LT2 with lysosome was markedly impaired, whereas S. typhi 1079 did not inhibit phagosome-lysosome fusion in murine macrophages. A similar inhibition of fusion was observed with LPS-deficient mutants of S. typhimurium LT2, suggesting that O-antigens do not contribute to the inhibition of fusion. Phagosome-lysosome fusion in macrophages after ingestion of UV-killed S. typhimurium LT2 was much greater than that of live bacteria. Furthermore, treatment of S. typhimurium LT2 with streptomycin, an inhibitor of bacterial protein synthesis, caused an increase in the extent of phagosome-lysosome fusion. Therefore protein synthesis in live bacteria is probably required for the inhibition of phagosome-lysosome fusion. These results suggest that phagosome-lysosome fusion in murine macrophages is impaired by some product(s) of viable S. typhimurium LT2.
对感染鼠伤寒沙门氏菌LT2或伤寒沙门氏菌1079的小鼠巨噬细胞中的吞噬体-溶酶体融合进行了研究。含有鼠伤寒沙门氏菌LT2的吞噬体与溶酶体的融合明显受损，而伤寒沙门氏菌1079并不抑制小鼠巨噬细胞中的吞噬体-溶酶体融合。用鼠伤寒沙门氏菌LT2的LPS缺陷突变体观察到了类似的融合抑制，这表明O抗原对融合抑制没有作用。摄入紫外线灭活的鼠伤寒沙门氏菌LT2后巨噬细胞中的吞噬体-溶酶体融合比活细菌的融合要大得多。此外，用链霉素（一种细菌蛋白质合成抑制剂）处理鼠伤寒沙门氏菌LT2会导致吞噬体-溶酶体融合程度增加。因此，活细菌中的蛋白质合成可能是抑制吞噬体-溶酶体融合所必需的。这些结果表明，鼠伤寒沙门氏菌LT2的某些活产物会损害小鼠巨噬细胞中的吞噬体-溶酶体融合。
