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SlyA, a transcriptional regulator of Salmonella typhimurium, is required for resistance to oxidative stress and is expressed in the intracellular environment of macrophages.

TitleSlyA, a transcriptional regulator of Salmonella typhimurium, is required for resistance to oxidative stress and is expressed in the intracellular environment of macrophages.
Publication TypeJournal Article
Year of Publication1997
AuthorsBuchmeier, N, Bossie, S, Chen, CY, Fang, FC, Guiney, DG, Libby, SJ
JournalInfect Immun
Volume65
Issue9
Pagination3725-30
Date Published1997 Sep
ISSN0019-9567
KeywordsAnimals, Bacterial Proteins, Bacterial Toxins, Cells, Cultured, Gene Expression Regulation, Bacterial, Hemolysin Proteins, Hydrogen Peroxide, Macrophages, Mice, Nitric Oxide, Oxidation-Reduction, Oxidative Stress, Paraquat, Reactive Oxygen Species, Salmonella typhimurium, Transcription Factors
Abstract

Appropriate regulation of genes enables Salmonella typhimurium to adapt to the intracellular environment of the host. The Salmonella slyA gene is in a family of transcriptional regulators that may play an important role in this adaptation. We have previously shown that slyA mutant Salmonella strains are profoundly attenuated for virulence and do not survive in macrophages. In this study, we demonstrate that the expression of multiple Salmonella proteins is regulated by SlyA during stationary phase and during infection of macrophages. Both of these conditions also induced the expression of a slyA::lacZ transcriptional fusion. Expression of the slyA::lacZ transcriptional fusion increased 15-fold in stationary phase and was not dependent on the stationary-phase sigma factor, RpoS. slyA mutant Salmonella strains were sensitive to oxidative products of the respiratory burst, including hydrogen peroxide and the products of the redox cycling compound paraquat, but not to nitric oxide donors. These results suggest that the SlyA regulon is activated during infection of the host and is required for resistance to toxic oxidative products of the reticuloendothelial system.

Alternate JournalInfect. Immun.
PubMed ID9284144
PubMed Central IDPMC175531
Grant ListAI32463 / AI / NIAID NIH HHS / United States
AI34397 / AI / NIAID NIH HHS / United States
AI39557 / AI / NIAID NIH HHS / United States