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K54荚膜多糖的存在会增加大肠杆菌在体内的致病性。

The presence of K54 capsular polysaccharide increases the pathogenicity of Escherichia coli in vivo.

作者信息

Russo T A, Liang Y, Cross A S

机构信息

Bacterial Pathogenesis Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland 20892.

出版信息

J Infect Dis. 1994 Jan;169(1):112-8. doi: 10.1093/infdis/169.1.112.

DOI:10.1093/infdis/169.1.112
PMID:8277173
Abstract

Proven isogenic capsule-negative derivatives (CP9.29, CP9.108, CP9.137, CP9.171, CP9.443, and CP9.C56), generated from an O4/K54/H5 blood isolate (CP9) of Escherichia coli by IS50L::phoA (TnphoA)-mediated transposon mutagenesis, were used to assess the function of a non-K1 capsule in three animal models. Intraperitoneal injection of CP9 (K54+) into mice resulted in an LD50 at 24 h of 5.5 x 10(6) cfu compared with LD50s of 2.6 x 10(7) cfu and 3.8 x 10(7) cfu for CP9.108 (K54-) and CP9.C56 (K54-) (P < .001). CP9 was cleared less rapidly from the bloodstream, after intravascular injection, than was CP9.108 (P < .01). In the rat granuloma pouch model, CP9 could proliferate from starting inocula as low as 1.0 x 10(3) cfu/mL. In contrast, capsule-deficient derivatives underwent transient log kills with starting inocula as high as 1.0 x 10(6) cfu/mL. Because proven isogenic strains were evaluated, a clear contribution of the K54 capsular polysaccharide to virulence in vivo is demonstrated.

摘要

通过IS50L::phoA(TnphoA)介导的转座子诱变从大肠杆菌的O4/K54/H5血液分离株(CP9)产生的经证实的同基因无荚膜衍生物(CP9.29、CP9.108、CP9.137、CP9.171、CP9.443和CP9.C56),用于在三种动物模型中评估非K1荚膜的功能。与CP9.108(K54-)和CP9.C56(K54-)的半数致死剂量2.6×10⁷ cfu和3.8×10⁷ cfu相比,腹腔注射CP9(K54+)到小鼠体内在24小时时的半数致死剂量为5.5×10⁶ cfu(P <.001)。血管内注射后,CP9从血液中清除的速度比CP9.108慢(P <.01)。在大鼠肉芽肿袋模型中,CP9可以从低至1.0×10³ cfu/mL的起始接种量增殖。相比之下,无荚膜缺陷衍生物在起始接种量高达1.0×10⁶ cfu/mL时经历短暂的对数杀灭。由于评估了经证实的同基因菌株,因此证明了K54荚膜多糖对体内毒力有明确贡献。

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1
The presence of K54 capsular polysaccharide increases the pathogenicity of Escherichia coli in vivo.K54荚膜多糖的存在会增加大肠杆菌在体内的致病性。
J Infect Dis. 1994 Jan;169(1):112-8. doi: 10.1093/infdis/169.1.112.
2
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