Glucose 6-phosphate dehydrogenase is required for Salmonella typhimurium virulence and resistance to reactive oxygen and nitrogen intermediates

Salmonella typhimurium zwf mutants lacking glucose 6-phosphate dehydrogenase (G6PD) activity have increased susceptibility to reactive oxygen and nitrogen intermediates as well as attenuated virulence in mice. Abrogation of the phagocyte respiratory burst oxidase during experimental infection with z...

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Bibliographic Details
Published in:Infection and immunity 1999, Vol.67 (1), p.436-438
Main Authors: LUNDBERG, B. E, WOLF, R. E, DINAUER, M. C, YISHENG XU, FANG, F. C
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
Bacteriology
Biological and medical sciences
Female
Fundamental and applied biological sciences. Psychology
Glucosephosphate Dehydrogenase - metabolism
Glucosephosphate Dehydrogenase - physiology
Glutathione - analogs & derivatives
Glutathione - pharmacology
Hydrogen Peroxide - pharmacology
Mice
Mice, Inbred C57BL
Mice, Knockout
Microbiology
Molecular and Cellular Pathogenesis
Nitrogen - metabolism
Nitroso Compounds - pharmacology
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Phagocytes - drug effects
Phagocytes - metabolism
Phagocytes - microbiology
Reactive Oxygen Species - metabolism
S-Nitrosoglutathione
Salmonella typhimurium
Salmonella typhimurium - drug effects
Salmonella typhimurium - enzymology
Salmonella typhimurium - pathogenicity
Virulence
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Summary:Salmonella typhimurium zwf mutants lacking glucose 6-phosphate dehydrogenase (G6PD) activity have increased susceptibility to reactive oxygen and nitrogen intermediates as well as attenuated virulence in mice. Abrogation of the phagocyte respiratory burst oxidase during experimental infection with zwf mutant Salmonella causes a prompt restoration of virulence, while inhibition of inducible nitric oxide synthase results in delayed lethality. These observations suggest that G6PD-dependent bacterial antioxidant defenses play an important pathogenic role during early salmonellosis and additionally may help to antagonize NO-dependent antimicrobial mechanisms later in the course of infection.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.67.1.436-438.1999