Karlsson-Kanth Anna, Tegmark-Wisell Karin, Arvidson Staffan, Oscarsson Jan
Microbiology and Tumor Biology Center (MTC), Box 280, Karolinska Institutet, S-17177 Stockholm, Sweden.
Int J Med Microbiol. 2006 Aug;296(4-5):229-36. doi: 10.1016/j.ijmm.2006.01.067. Epub 2006 Mar 10.
It has been reported that high production of proteases and alpha-hemolysin in the prototype Staphylococcus aureus strain 8325-4 was associated with its sigmaB deficiency. Here we analyzed one fresh clinical isolate (KS26) and two ancient human isolates (Wood46 and V8) selected for high production of proteases and alpha-hemolysin. All three strains lacked yellow pigment and showed a low level of expression of sigB-dependent promoters, indicating sigmaB deficiency. Nucleotide sequencing of the sigB operon revealed that KS26 and Wood46 had stop codons in rsbU and sigB, respectively, while V8 had an insertion of an IS element in rsbU. Complementation experiments with sigB on a plasmid reduced expression of proteases and alpha-hemolysin dramatically, indicating that the high production of these exoproteins was associated with sigmaB deficiency. Although sigmaB-deficient strains show attenuated virulence in some animal models, our results indicate that such strains can cause infection in humans.
据报道，金黄色葡萄球菌原型菌株8325-4中蛋白酶和α-溶血素的高产量与其σB缺陷有关。在此，我们分析了一株新的临床分离株（KS26）和两株因蛋白酶和α-溶血素高产量而被挑选出的古老人类分离株（Wood46和V8）。所有三株菌株均缺乏黄色色素，且显示出sigB依赖性启动子的低表达水平，表明存在σB缺陷。σB操纵子的核苷酸测序显示，KS26和Wood46分别在rsbU和sigB中有终止密码子，而V8在rsbU中有一个IS元件插入。用质粒上的sigB进行互补实验显著降低了蛋白酶和α-溶血素的表达，表明这些胞外蛋白的高产量与σB缺陷有关。尽管σB缺陷菌株在一些动物模型中显示出毒力减弱，但我们的结果表明，此类菌株可导致人类感染。
