Charnetzky W T, Shuford W W
Infect Immun. 1985 Jan;47(1):234-41. doi: 10.1128/iai.47.1.234-241.1985.
The survival and growth of Yersinia pestis cells within mouse peritoneal cavities and within mouse peritoneal macrophages maintained in vitro was examined. Two strains were used which differed only in that one (KIM) contained the 47-megadalton plasmid associated with virulence and the second (KIM1) lacked this plasmid. The KIM cells, but not the KIM1 cells, acquired some resistance to phagocytosis during growth at 37 degrees C which was not evident when cells were grown at 26 degrees C. Whether previously grown at 26 or 37 degrees C, however, a substantial portion of the cells of either strain which were phagocytized were apparently killed after phagocytosis in vivo, although this was not observed in vitro. KIM cells which survived phagocytosis proliferated within macrophages in vivo, but no increase in viable cells was seen with the KIM1 cells. Growth of the KIM1 cells within macrophages in vitro required that a complex supportive medium be used in which the bacteria could have grown if extracellular. This was not the case for the KIM cells which proliferated within macrophages supported in medium not permissive to bacterial growth. After phagocytosis of cells of either strain by macrophages maintained in vitro, phagolysosome formation occurred normally, as shown by the acridine orange dye staining technique. KIM and KIM1 cells were equally sensitive to hydrogen peroxide and superoxide anion, although the sensitivity in each case varied with growth temperature. The oxidative burst, as determined by the luminol chemiluminescence assay, was low when compared with that seen after phagocytosis of Escherichia coli cells. Chemiluminescence after phagocytosis of yeast cells by macrophages which had engulfed KIM or KIM1 was also low. We conclude that survival within macrophages is substantially independent of the 47-megadalton plasmid and may be a consequence, as least in part, of blockage of the oxidative burst or rapid removal of the oxidizing compounds formed. The 47-megadalton plasmid is apparently required for subsequent proliferation within the macrophage.
研究了鼠疫耶尔森氏菌细胞在小鼠腹腔内以及体外培养的小鼠腹腔巨噬细胞内的存活和生长情况。使用了两种菌株,它们的区别仅在于一种(KIM)含有与毒力相关的47兆道尔顿质粒,而另一种(KIM1)缺乏该质粒。KIM细胞在37℃生长期间获得了一定的抗吞噬能力,而在26℃生长时则不明显,KIM1细胞则没有这种情况。然而,无论之前是在26℃还是37℃生长,两种菌株中被吞噬的大部分细胞在体内吞噬后显然都被杀死了,尽管在体外未观察到这种情况。在体内吞噬后存活的KIM细胞在巨噬细胞内增殖,但KIM1细胞的活细胞数量未见增加。KIM1细胞在体外巨噬细胞内生长需要使用复杂的支持培养基,如果是细胞外生长,细菌可以在这种培养基中生长。而KIM细胞在不允许细菌生长的培养基支持的巨噬细胞内增殖时则并非如此。用吖啶橙染色技术显示,体外培养的巨噬细胞吞噬任何一种菌株的细胞后,吞噬溶酶体的形成正常。KIM和KIM1细胞对过氧化氢和超氧阴离子同样敏感,尽管每种情况下的敏感性随生长温度而变化。与吞噬大肠杆菌细胞后观察到的情况相比,通过鲁米诺化学发光测定法测定的氧化爆发较低。吞噬了KIM或KIM1的巨噬细胞吞噬酵母细胞后的化学发光也较低。我们得出结论认为,在巨噬细胞内的存活基本上与47兆道尔顿质粒无关,可能至少部分是氧化爆发受阻或形成的氧化化合物被快速清除的结果。47兆道尔顿质粒显然是随后在巨噬细胞内增殖所必需的。