Ugalde J E, Czibener C, Feldman M F, Ugalde R A
Instituto de Investigaciones Biotecnológicas-Instituto Tecnológico de Chascomús, Universidad Nacional de General San Martín, Buenos Aires, Argentina.
Infect Immun. 2000 Oct;68(10):5716-23. doi: 10.1128/IAI.68.10.5716-5723.2000.
Smooth lipopolysaccharide (LPS) of Brucella abortus has been reported to be an important virulence factor, although its precise role in pathogenesis is not yet clear. While the protective properties of LPS against complement are well accepted, there is still some controversy about the capacity of rough mutants to replicate intracellularly. The B. abortus phosphoglucomutase gene (pgm) was cloned, sequenced, and disrupted. The gene has a high index of identity to Agrobacterium tumefaciens pgm but is not part of the glycogen operon. A B. abortus null mutant lacks LPS O antigen but has an LPS core with an electrophoretic profile undistinguishable from that of the wild-type core, suggesting that glucose, galactose, or a derivative of these sugars may be part of the linkage between the core and the O antigen. This mutant is unable to survive in mice but replicates in HeLa cells, indicating that the complete LPS is not essential either for invasion or for intracellular multiplication. This behavior suggests that the LPS may play a role in extracellular survival in the animal, probably protecting the cell against complement-mediated lysis, but is not involved in intracellular survival.
流产布鲁氏菌的光滑型脂多糖(LPS)据报道是一种重要的毒力因子,尽管其在发病机制中的确切作用尚不清楚。虽然LPS对补体的保护特性已得到广泛认可,但关于粗糙突变体在细胞内复制能力仍存在一些争议。流产布鲁氏菌磷酸葡萄糖变位酶基因(pgm)被克隆、测序并破坏。该基因与根癌土壤杆菌的pgm具有高度同源性,但不是糖原操纵子的一部分。流产布鲁氏菌缺失突变体缺乏LPS O抗原,但具有与野生型核心电泳图谱无法区分的LPS核心,这表明葡萄糖、半乳糖或这些糖的衍生物可能是核心与O抗原之间连接的一部分。该突变体在小鼠中无法存活,但能在HeLa细胞中复制,这表明完整的LPS对于侵袭或细胞内增殖并非必不可少。这种行为表明LPS可能在动物的细胞外存活中起作用,可能保护细胞免受补体介导的裂解,但不参与细胞内存活。