Caron E, Cellier M, Liautard J P, Köhler S
Institut National de la Santé et de la Recherche Médicale U-65, Dept. Biologie-Santé, Université Montpellier II, France.
FEMS Microbiol Lett. 1994 Jul 15;120(3):335-40. doi: 10.1111/j.1574-6968.1994.tb07055.x.
Facultatively intracellular bacteria express heat shock proteins after phagocytosis by macrophages. Using non-pathogenic Escherichia coli strains and the human monocytic cell line U937, we showed that deletion of the dnaK gene significantly increased the rate of initial intracellular killing of bacteria. Trans-complementation of the deletion mutant with the dnaK/dnaJ operon of Brucella ovis restored the pattern of intracellular elimination of the control strain expressing dnaK. These differences were not observed using antibody-opsonized bacteria and activated cells. In vitro, strains expressing dnaK resisted hydrogen peroxide better than the deletion mutant; in contrast, the mutant complemented by dnaK/dnaJ of B. ovis tolerated low pH and low H2O2 better than the wild-type strain and the deletion mutant. Our results suggested the participation of DnaK in protection of intracellular bacteria against antimicrobial macrophage factors.
兼性胞内菌在被巨噬细胞吞噬后会表达热休克蛋白。利用非致病性大肠杆菌菌株和人单核细胞系U937，我们发现dnaK基因的缺失显著提高了细菌最初的胞内杀伤率。用绵羊布鲁氏菌的dnaK/dnaJ操纵子对缺失突变体进行反式互补，恢复了表达dnaK的对照菌株的胞内清除模式。使用抗体调理的细菌和活化细胞时未观察到这些差异。在体外，表达dnaK的菌株比缺失突变体对过氧化氢的抵抗力更强；相反，用绵羊布鲁氏菌的dnaK/dnaJ互补的突变体比野生型菌株和缺失突变体更能耐受低pH值和低浓度的过氧化氢。我们的结果表明DnaK参与了保护胞内细菌免受巨噬细胞抗菌因子的作用。
