Evidence map›Paper›PMID 27354296›Full record

ReviewPathogens and disease2016

Neutrophil-generated oxidative stress and protein damage in Staphylococcus aureus.

William N Beavers, Eric P Skaar

Open access · bronzeAbstract readReview
In one paragraph

Review in Pathogens and disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.5field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

75 citing papers in PubMed, 121 citations in OpenAlex.

  1. Fibroblasts resistScience advances · 2026
    Article
  2. Article
  3. Article
  4. Foods (Basel, Switzerland) · 2025
    Article
  5. Myeloperoxidase as a therapeutic target for oxidative damage in Alzheimer's disease.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  6. Article
  7. Review
  8. Safety trial assessing 1.77 cmScientific reports · 2025
    Article
  9. Defects in anaplerotic metabolism sensitizeMicrobiology spectrum · 2025
    Article
  10. Review
  11. Article
  12. Microneedle Patch for In Situ Neutrophil Monitoring.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  13. What Do We Know AboutToxics · 2025
    Review
  14. Pathogens (Basel, Switzerland) · 2025
    Review
  15. Article
  16. Neutrophils in Atopic Dermatitis.Clinical reviews in allergy & immunology · 2024
    Review
  17. Article
  18. Infection and immunity · 2024
    Article
  19. Review
  20. Article

15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

William N BeaversDepartment of Pathology, Microbiology and Immunology, U.S. Department of Veteran Affairs, Vanderbilt Institute of Chemical Biology, Vanderbilt University School of Medicine, 1161 21st Avenue South, Medical Center North, Nashville, TN 37232, USA.
Eric P SkaarDepartment of Pathology, Microbiology and Immunology, U.S. Department of Veteran Affairs, Vanderbilt Institute of Chemical Biology, Vanderbilt University School of Medicine, 1161 21st Avenue South, Medical Center North, Nashville, TN 37232, USA Tennessee Valley Healthcare System, U.S. Department of Veteran Affairs, Vanderbilt Institute of Chemical Biology, Vanderbilt University School of Medicine, 1161 21st Avenue South, Nashville, TN 37232, USA eric.skaar@vanderbilt.edu.
Vanderbilt University · USVA Tennessee Valley Healthcare System · US

Funding

Vanderbilt Infection Pathogenesis and Epidemiology Research Training ProgramT32AI007474 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KALAMS, SPYROS A · 1995 to 2025
$6.9M
Pathobiology of heme inducible transporters in Gram positive pathogensR01AI073843 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SKAAR, ERIC P · 2009 to 2025
$5.9M
NIAID NIH HHS R01 AI073843
6 · The paper itself

Abstract

Staphylococcus aureus is a ubiquitous, versatile and dangerous pathogen. It colonizes over 30% of the human population, and is one of the leading causes of death by an infectious agent. During S. aureus colonization and invasion, leukocytes are recruited to the site of infection. To combat S. aureus, leukocytes generate an arsenal of reactive species including superoxide, hydrogen peroxide, nitric oxide and hypohalous acids that modify and inactivate cellular macromolecules, resulting in growth defects or death. When S. aureus colonization cannot be cleared by the immune system, antibiotic treatment is necessary and can be effective. Yet, this organism quickly gains resistance to each new antibiotic it encounters. Therefore, it is in the interest of human health to acquire a deeper understanding of how S. aureus evades killing by the immune system. Advances in this field will have implications for the design of future S. aureus treatments that complement and assist the host immune response. In that regard, this review focuses on how S. aureus avoids host-generated oxidative stress, and discusses the mechanisms used by S. aureus to survive oxidative damage including antioxidants, direct repair of damaged proteins, sensing oxidant stress and transcriptional changes. This review will elucidate areas for studies to identify and validate future antimicrobial targets.

Indexed as

Host-Pathogen InteractionsOxidative StressAnimalsGene Expression RegulationHumansMicrobial ViabilityNeutrophilsNitric OxideOxidantsOxidation-ReductionRespiratory BurstStaphylococcal InfectionsStaphylococcus aureusNitric OxideOxidantsantioxidant defenseshost–pathogen interfaceneutrophilsoxidative stressprotein oxidationStaphylococcus aureus

Identifiers

PMID27354296
PMCPMC5975594
OpenAlexW2474720808

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.