Evidence map›Paper›PMID 22393157›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Extracellular superoxide dismutase inhibits innate immune responses and clearance of an intracellular bacterial infection.

Timothy J Break, Sujung Jun, Mohanalaxmi Indramohan, Karen D Carr, Amy N Sieve, Ladislav Dory, Rance E Berg

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Superoxide Radicals in the Execution of Cell Death.Antioxidants (Basel, Switzerland) · 2022
    Review
  5. Article
  6. Neutrophils: Many Ways to Die.Frontiers in immunology · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Innate and Adaptive Immune Responses duringMicrobiology spectrum · 2019
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Timothy J BreakDepartment of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Sujung Jun
Mohanalaxmi Indramohan
Karen D Carr
Amy N Sieve
Ladislav Dory
Rance E Berg
University of North Texas Health Science Center · USUniversity of North Texas · US

Funding

Hyperbaric oxygen and atherosclerosisR01HL070599 · NHLBI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI DORY, LADISLAV · 2004 to 2007
$1.5M
Regulation of Immune Responses by interleukin-23F32AI072946 · NIAID · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SIEVE, AMY NICOLE · 2008 to 2010
$157k
NHLBI NIH HHS R01 HL070599NHLBI NIH HHS R01 HL70599NIAID NIH HHS F32 AI072946
6 · The paper itself

Abstract

Reactive oxygen species and reactive nitrogen species play important roles during immune responses to bacterial pathogens. Extracellular superoxide dismutase (ecSOD) regulates extracellular concentrations of reactive oxygen species and reactive nitrogen species and contributes to tissue protection during inflammatory insults. The participation of ecSOD in immune responses seems therefore intuitive, yet is poorly understood. In the current study, we used mice with varying levels of ecSOD activity to investigate the involvement of this enzyme in immune responses against Listeria monocytogenes. Surprisingly, our data demonstrate that despite enhanced neutrophil recruitment to the liver, ecSOD activity negatively affected host survival and bacterial clearance. Increased ecSOD activity was accompanied by decreased colocalization of neutrophils with bacteria, as well as increased neutrophil apoptosis, which reduced overall and neutrophil-specific TNF-α production. Liver leukocytes from mice lacking ecSOD produced equivalent NO· compared with liver leukocytes from mice expressing ecSOD. However, during infection, there were higher levels of peroxynitrite (NO(3)·(-)) in livers from mice lacking ecSOD compared with livers from mice expressing ecSOD. Neutrophil depletion studies revealed that high levels of ecSOD activity resulted in neutrophils with limited protective capacity, whereas neutrophils from mice lacking ecSOD provided superior protection compared with neutrophils from wild-type mice. Taken together, our data demonstrate that ecSOD activity reduces innate immune responses during bacterial infection and provides a potential target for therapeutic intervention.

Indexed as

AnimalsApoptosisChemotaxis, LeukocyteDisease SusceptibilityEnzyme InductionFemaleHost-Pathogen InteractionsImmunity, InnateListeria monocytogenesListeriosisLiverLymphocyte SubsetsMaleMiceMice, CongenicMice, Inbred C57BLNitric OxidePeroxynitrous AcidReactive Nitrogen SpeciesReactive Oxygen SpeciesSod3 protein, mouseSuperoxide DismutaseTumor Necrosis Factor-alpha

Identifiers

PMID22393157
PMCPMC3311725
OpenAlexW2151156869

What OpenQuestion holds

Textmetadata
LicenceTDM
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.