Expression of katG in Mycobacterium tuberculosis is associated with its growth and persistence in mice and guinea pigs

被引：142

作者：

Li, ZM ^{[1
]}

Kelley, C ^{[1
]}

Collins, F ^{[1
]}

Rouse, D ^{[1
]}

Morris, S ^{[1
]}

机构：

[1] US FDA, CDER, Lab Mycobacteria, Rockville, MD 20857 USA

来源：

JOURNAL OF INFECTIOUS DISEASES | 1998年 / 177卷 / 04期

关键词：

D O I：

10.1086/515254

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

The molecular mechanisms associated with the pathogenesis of tuberculosis are not well understood. The present study evaluated the role of catalase-peroxidase as a potential virulence factor for Mycobacterium tuberculosis. Growth and persistence of M. tuberculosis H37Rv in intravenously infected BALB/c mice were compared with katG-deleted, isoniazid-resistant M. tuberculosis H37RvINH(R). Transformation of M. tuberculosis H37Rv (TBkatG) or Mycobacterium intracellulare (MACkatG) genes into M. tuberculosis H37RvINH(R) restored its catalase-peroxidase activities and the ability of the recombinants to persist in spleens of mice and guinea pigs. Transformation with the TBkatG gene with the codon 463 R-->L mutation also restored catalase-peroxidase activity and enhanced persistence. However, transformants with the codon 275 T-->P mutant expressed low levels of enzymatic activity and failed to persist in guinea pig spleen, although they did survive in mouse tissues. These results indicate that KatG contributes to the ability of M. tuberculosis to grow and survive within the infected host tissues.

引用

页码：1030 / 1035

页数：6

共 33 条

[11] Effects of overexpression of the alkyl hydroperoxide reductase AhpC on the virulence and isoniazid resistance of Mycobacterium tuberculosis [J].