Goldberg J B, Coyne M J, Neely A N, Holder I A
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Infect Immun. 1995 Oct;63(10):4166-9. doi: 10.1128/iai.63.10.4166-4169.1995.
The virulence of wild-type Pseudomonas aeruginosa PAO1 and that of a genetically defined algC mutant, PAO1 algC::tet, were compared in a burned-mouse model of infection. Unlike PAO1, PAO1 algC::tet was avirulent, grew less well in the eschar, and did not disseminate to the liver of challenged animals. We have previously shown that the P. aeruginosa algC gene is required for biosynthesis of alginate and lipopolysaccharide (M.J. Coyne, Jr., K.S. Russell, C.L. Coyle, and J.B. Goldberg, J. Bacteriol. 176:3500-3507, 1994). In order to determine whether the alginate or lipopolysaccharide (LPS) defect was responsible for the avirulence of this strain, we constructed a strain with a mutation in an alginate-specific gene, algD. PAO1-algD was virulent in the burned-mouse model, thus implicating the LPS defect in PAO1 algC::tet as the relevant alteration responsible for the avirulence of this strain.
在烧伤小鼠感染模型中，对野生型铜绿假单胞菌PAO1和基因明确的algC突变体PAO1 algC::tet的毒力进行了比较。与PAO1不同，PAO1 algC::tet无毒力，在焦痂中生长较差，并且不会扩散到受攻击动物的肝脏。我们之前已经表明，铜绿假单胞菌algC基因是藻酸盐和脂多糖生物合成所必需的（M.J. Coyne, Jr., K.S. Russell, C.L. Coyle, and J.B. Goldberg, J. Bacteriol. 176:3500 - 3507, 1994）。为了确定藻酸盐或脂多糖（LPS）缺陷是否是该菌株无毒力的原因，我们构建了一个在藻酸盐特异性基因algD中发生突变的菌株。PAO1-algD在烧伤小鼠模型中具有毒力，因此表明PAO1 algC::tet中的LPS缺陷是导致该菌株无毒力的相关改变。
