Wanken Amy E, Conway Tyrrell, Eaton Kathryn A
Department of Veterinary Biosciences, Ohio State University, Columbus, Ohio 43210, USA.
Infect Immun. 2003 May;71(5):2920-3. doi: 10.1128/IAI.71.5.2920-2923.2003.
Helicobacter pylori mutants deficient in 6-phosphogluconate dehydratase (6PGD) were constructed. Colonization densities were lower and minimum infectious doses were higher for mutant strains than for wild-type strains. In spite of better colonization, however, wild-type strains did not displace the mutant in cocolonization experiments. Loss of 6PGD diminishes the fitness of H. pylori in vivo, but the pathway is nonessential for colonization.
构建了缺乏6-磷酸葡萄糖酸脱水酶（6PGD）的幽门螺杆菌突变体。与野生型菌株相比，突变株的定殖密度较低，最小感染剂量较高。然而，尽管野生型菌株定殖能力更强，但在共定殖实验中，野生型菌株并未取代突变体。6PGD的缺失降低了幽门螺杆菌在体内的适应性，但该途径对于定殖并非必不可少。
