期刊
INFECTION AND IMMUNITY
卷 73, 期 8, 页码 4581-4587出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.73.8.4581-4587.2005
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资金
- NHLBI NIH HHS [HL61241] Funding Source: Medline
- NIAID NIH HHS [T32 AI007621, AI055548, T32 AI07621] Funding Source: Medline
Mutations in Mycobacterium tuberculosis uvrB result in severe sensitivity to acidified nitrite, a source of nitric oxide (6). In this study, we show that a uvrB mutant is exquisitely sensitive to UV light but not to several sources of reactive oxygen species in vitro. Furthermore, a uvrB mutant was attenuated in mice as judged by an extension of life span. Attenuation in mice was partially reversed by genetic inactivation of nitric oxide synthase 2 (iNOS) and almost completely reversed in mice lacking both iNOS and phagocyte oxidase. Thus, a gene predicted to encode a key element of DNA repair is required for resistance of M. tuberculosis to both reactive nitrogen and reactive oxygen species in mice.
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