Department of Microbiological Chemistry, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Infect Immun. 1970 Mar;1(3):305-10. doi: 10.1128/iai.1.3.305-310.1970.
Wild-type Salmonella typhimurium and cell wall mutants with sequential deficiencies in their cell wall polysaccharide were examined for sensitivity to the bactericidal action of the lysosomal fraction of polymorphonuclear leukocytes. The complete lipopolysaccharide basal core was essential for resistance to the bactericidal action. O-specific side chains of the wild type did not enhance the resistance. Absence of N-acetyl glucosamine considerably enhanced sensitivity, whereas absence of other core sugars did not; additional increase in sensitivity was obtained when the heptose phosphate was absent. Under conditions where appropriate supplementation of the medium permitted complete cell wall synthesis, the uridine diphosphate-gal-4-epimeraseless mutant regained resistance that was essentially equal to that of the wild type. Cells coated with specific antiserum and nongrowing cells were more resistant than normal growing cells.
野生型鼠伤寒沙门氏菌和细胞壁突变体，其细胞壁多糖依次缺乏，对多形核白细胞溶酶体部分的杀菌作用的敏感性进行了检查。完整的脂多糖基础核心对于抵抗杀菌作用是必需的。O 型特异性侧链对野生型没有增强抗性。缺乏 N-乙酰葡萄糖胺会大大增加敏感性，而其他核心糖的缺失则不会；当庚糖磷酸不存在时，敏感性会进一步增加。在适当补充培养基的条件下，允许完全细胞壁合成的情况下，尿嘧啶二磷酸半乳糖-4-差向异构酶缺失突变体恢复了与野生型基本相等的抗性。用特异性抗血清包被的细胞和非生长细胞比正常生长细胞更具抗性。
