Infection and Immunity, January 1999, p. 436-438, Vol. 67, No. 1
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Departments of Medicine, Pathology, and Microbiology, University of Colorado Health Sciences Center, Denver, Colorado 802621; Department of Biological Sciences, University of Maryland Baltimore County, Baltimore, Maryland 212282; and Departments of Pediatrics and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana 462023
Received 12 August 1998/Returned for modification 28 September 1998/Accepted 10 October 1998
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.
Present address: Department of Medicine, Emory School of Medicine,
Atlanta, GA 30308.
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