Activation by nitric oxide of an oxidative-stress response that defends Escherichia coli against activated macrophages

التفاصيل البيبلوغرافية
العنوان: Activation by nitric oxide of an oxidative-stress response that defends Escherichia coli against activated macrophages
المؤلفون: Teresa deRojas-Walker, Bruce Demple, Steven R. Tannenbaum, John S. Wishnok, Tatsuo Nunoshiba
المصدر: Proceedings of the National Academy of Sciences. 90:9993-9997
بيانات النشر: Proceedings of the National Academy of Sciences, 1993.
سنة النشر: 1993
مصطلحات موضوعية: Xanthine Oxidase, Mice, Inbred Strains, Nitric Oxide, Regulon, Gene Expression Regulation, Enzymologic, Nitric oxide, Superoxide dismutase, Mice, chemistry.chemical_compound, Superoxides, Operon, Escherichia coli, Animals, Cloning, Molecular, chemistry.chemical_classification, Hypoxanthine, Reactive oxygen species, Multidisciplinary, biology, Superoxide Dismutase, Superoxide, Macrophages, Nitric oxide dioxygenase, Gene Expression Regulation, Bacterial, Hydrogen Peroxide, Macrophage Activation, Cytostasis, Respiratory burst, Biochemistry, chemistry, Genes, Bacterial, Enzyme Induction, Hypoxanthines, biology.protein, Female, Bacterial outer membrane, Research Article
الوصف: Nitric oxide is a free radical (NO) formed biologically through the oxidation of L-arginine by nitric oxide synthases. NO is produced transiently in mammalian cells for intercellular signaling and in copious quantities to cause cytostasis and cytotoxicity. In the latter situation, NO is a deliberate cytotoxic product of activated macrophages, along with other reactive oxygen species such as hydrogen peroxide (H2O2) and superoxide (O2-). Escherichia coli has a complex set of responses to H2O2 and O2- that involves approximately 80 inducible proteins; we wondered whether these bacteria might induce analogous defenses against nitric oxide. We show here that a multigene system controlled by the redox-sensitive transcriptional regulator SoxR is activated by NO in vivo. This induction confers bacterial resistance to activated murine macrophages with kinetics that parallel the production of NO by these cells. Elimination of specific SoxR-regulated genes diminishes the resistance of these bacteria to the cytotoxic macrophages. The required functions include manganese-containing superoxide dismutase, endonuclease IV (a DNA-repair enzyme for oxidative damage), and micF, an antisense regulator of the outer membrane porin OmpF. These results demonstrate that SoxR is a sensor for cellular exposure to NO, and that the soxRS response system may contribute to bacterial virulence.
تدمد: 1091-6490
0027-8424
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f90c8ffa0ca7e63ee10ab03b42174543
https://doi.org/10.1073/pnas.90.21.9993
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....f90c8ffa0ca7e63ee10ab03b42174543
قاعدة البيانات: OpenAIRE