Ishibashi Y, Arai T
Department of Microbiology, Meiji College of Pharmacy, Nozawa, Tokyo, Japan.
FEMS Microbiol Immunol. 1989 Apr;1(5):279-84. doi: 10.1111/j.1574-6968.1989.tb02393.x.
The susceptibility of Salmonella typhimurium LT2 and S. typhi 1079 to oxygen metabolites were compared. S. typhimurium LT2 and S. typhi 1079 were killed to an equal extent (about 40%) by the xanthine-xanthine oxidase (200 mU/ml) system. Among the various scavengers of oxygen metabolites, catalase alone inhibited the killing of S. typhimurium LT2 and S. typhi 1079 by the xanthine-xanthine oxidase system, indicating that hydrogen peroxide contributed to the killing of Salmonellae. The respiratory burst of murine macrophages was efficiently triggered by the ingestion of S. typhimurium LT2, S. typhimurium SL1102, and S. typhi 1079 and all to the same extent. However, in the range of the concentration of hydrogen peroxide produced by murine macrophages, neither S. typhimurium LT2 nor S. typhi 1079 were killed. Only S. typhimurium SL1102, a rough mutant of S. typhimurium LT2, was markedly susceptible under these conditions. The findings suggest that both S. typhimurium LT2 and S. typhi 1079 are resistant to oxygen-dependent killing mechanisms.
比较了鼠伤寒沙门氏菌LT2和伤寒沙门氏菌1079对氧代谢产物的敏感性。鼠伤寒沙门氏菌LT2和伤寒沙门氏菌1079被黄嘌呤-黄嘌呤氧化酶（200 mU/ml）系统同等程度地杀死（约40%）。在各种氧代谢产物清除剂中，仅过氧化氢酶抑制了黄嘌呤-黄嘌呤氧化酶系统对鼠伤寒沙门氏菌LT2和伤寒沙门氏菌1079的杀伤作用，表明过氧化氢参与了沙门氏菌的杀伤过程。鼠伤寒沙门氏菌LT2、鼠伤寒沙门氏菌SL1102和伤寒沙门氏菌1079的摄入均能有效触发小鼠巨噬细胞的呼吸爆发，且程度相同。然而，在小鼠巨噬细胞产生的过氧化氢浓度范围内，鼠伤寒沙门氏菌LT2和伤寒沙门氏菌1079均未被杀死。只有鼠伤寒沙门氏菌LT2的粗糙突变体鼠伤寒沙门氏菌SL1102在这些条件下明显敏感。这些发现表明，鼠伤寒沙门氏菌LT2和伤寒沙门氏菌1079均对氧依赖性杀伤机制具有抗性。
