ArticlePloS one2009
Phagocytic superoxide specifically damages an extracytoplasmic target to inhibit or kill Salmonella.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 95 citations in OpenAlex.
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- Ecotin protects Salmonella Typhimurium against the microbicidal activity of host proteases.PLoS pathogens · 2025Article
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- Amygdalin Reverses Macrophage PANoptosis Induced by Drug-ResistantJournal of microbiology and biotechnology · 2023Article
- Gre factors help Salmonella adapt to oxidative stress by improving transcription elongation and fidelity of metabolic genes.PLoS biology · 2023Article
- Biochemical Analysis ofACS infectious diseases · 2022Article
- When the Phagosome Gets Leaky: Pore-Forming Toxin-Induced Non-Canonical Autophagy (PINCA).Frontiers in cellular and infection microbiology · 2022Article
- Host Defense againstJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Functions of ROS in Macrophages and Antimicrobial Immunity.Antioxidants (Basel, Switzerland) · 2021Review
- Reactive Oxygen Species: Not Omnipresent but Important in Many Locations.Frontiers in cell and developmental biology · 2021Article
- How Microbes Defend Themselves From Incoming Hydrogen Peroxide.Frontiers in immunology · 2021Review
- Association of Virulence and Antibiotic Resistance inMicroorganisms · 2020Article
- Evolutionary causes and consequences of bacterial antibiotic persistence.Nature reviews. Microbiology · 2020Review
- Impact of small RNA RaoN on nitrosative-oxidative stress resistance and virulence of Salmonella enterica serovar Typhimurium.Journal of microbiology (Seoul, Korea) · 2020Article
- Glycolytic reprograming in Salmonella counters NOX2-mediated dissipation of ΔpH.Nature communications · 2020Article
- Modulation of Macrophage Function byFrontiers in cell and developmental biology · 2020Article
- Escaping the Phagocytic Oxidative Burst: The Role of SODB in the Survival ofFrontiers in microbiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe phagocytic oxidative burst is a primary effector of innate immunity that protects against bacterial infection. However, the mechanism by which reactive oxygen species (ROS) kill or inhibit bacteria is not known. It is often assumed that DNA is a primary target of oxidative damage, consistent with known effects of endogenously produced ROS in the bacterial cytoplasm. But most studies fail to distinguish between effects of host derived ROS versus damage caused by endogenous bacterial sources. We took advantage of both the ability of Salmonella enterica serovar Typhimurium to survive in macrophages and the genetic tractability of the system to test the hypothesis that phagocytic superoxide damages cytoplasmic targets including DNA. METHODOLOGY/PRINCIPAL
findingsSodCI is a periplasmic Cu-Zn superoxide dismutase (SOD) that contributes to the survival of Salmonella Typhimurium in macrophages. Through competitive virulence assays, we asked if sodCI has a genetic interaction with various cytoplasmic systems. We found that SodCI acts independently of cytoplasmic SODs, SodA and SodB. In addition, SodCI acts independently of the base excision repair system and RuvAB, involved in DNA repair. Although sodCI did show genetic interaction with recA, this was apparently independent of recombination and is presumably due to the pleiotropic effects of a recA mutation. CONCLUSIONS/SIGNIFICANCE: Taken together, these results suggest that bacterial inhibition by phagocytic superoxide is primarily the result of damage to an extracytoplasmic target.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.