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脂多糖的O4特异性抗原部分而非K54 2型荚膜对大肠埃希菌肠外分离株的尿路致病性很重要。

The O4 specific antigen moiety of lipopolysaccharide but not the K54 group 2 capsule is important for urovirulence of an extraintestinal isolate of Escherichia coli.

作者信息

Russo T, Brown J J, Jodush S T, Johnson J R

机构信息

Department of Medicine, State University of New York at Buffalo, USA.

出版信息

Infect Immun. 1996 Jun;64(6):2343-8. doi: 10.1128/iai.64.6.2343-2348.1996.

Abstract

Group 2 capsules and lipopolysaccharides are regarded as important virulence factors in extraintestinal isolates of Escherichia coli, but their specific contributions to bladder and renal infections, if any, are unknown. Proven isogenic derivatives deficient in the K54 antigen alone (CP9.137), the O4 antigen alone (CP921), or both the K54 and O4 antigens (CP923) were compared with their wild-type parent (CP9 [O4/K54JH5]) for growth in human urine in vitro and for virulence in vivo in a mouse model of ascending urinary tract infection (UTI). Growth of CP9.137 and CP921 was equivalent to that of CP9 in human urine. CP923 demonstrated a small but reproducible decrease in log-phase growth but achieved the same plateau density. In the mouse model of UTI, the isogenic mutant deficient in the 04 antigen alone (CP921) and, to a greater degree, the derivative deficient in both the K54 and O4 antigens (CP923) were significantly less virulent in nearly all parameters measured. In contrast, the K54 knockout derivative was as virulent as its parent, CP9, in causing bladder infection and nearly as virulent in causing renal infection. These results demonstrate an important role for the O4 antigen moiety of lipopolysaccharide in the pathogenesis of UTI. The possibility that the K54 antigen also plays a minor role cannot be excluded.

摘要

第2组荚膜和脂多糖被认为是大肠埃希菌肠外分离株中的重要毒力因子,但它们对膀胱和肾脏感染的具体作用(如果有的话)尚不清楚。将仅缺乏K54抗原(CP9.137)、仅缺乏O4抗原(CP921)或同时缺乏K54和O4抗原(CP923)的经证实的同基因衍生物与其野生型亲本(CP9 [O4/K54JH5])进行比较,以观察它们在人尿中的体外生长情况以及在小鼠上行性尿路感染(UTI)模型中的体内毒力。CP9.137和CP921在人尿中的生长情况与CP9相当。CP923在对数生长期的生长有小幅但可重复的下降,但达到了相同的平台期密度。在UTI小鼠模型中,仅缺乏O4抗原的同基因突变体(CP921)以及在更大程度上同时缺乏K54和O4抗原的衍生物(CP923)在几乎所有测量参数中的毒力均显著降低。相比之下,K54基因敲除衍生物在引起膀胱感染方面的毒力与其亲本CP9相当,在引起肾脏感染方面的毒力也几乎相当。这些结果表明脂多糖的O4抗原部分在UTI发病机制中起重要作用。不能排除K54抗原也起次要作用的可能性。

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