Evidence map›Paper›PMID 25385799›Full record

ArticleInfection and immunity2015

Neutralization of mitochondrial superoxide by superoxide dismutase 2 promotes bacterial clearance and regulates phagocyte numbers in zebrafish.

E M Peterman, C Sullivan, M F Goody, I Rodriguez-Nunez, J A Yoder, C H Kim

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Mitochondrial connections with immune system in Zebrafish.Fish and shellfish immunology reports · 2021
    Review
  14. Article
  15. Zebrafish as an animal model for biomedical research.Experimental & molecular medicine · 2021
    Review
  16. Article
  17. Zebrafish Embryo Infection Model to InvestigateFrontiers in cellular and infection microbiology · 2021
    Review
  18. Review
  19. Review
  20. Review
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

6 authors at 2 institutions in 1 country.

E M PetermanDepartment of Molecular and Biomedical Sciences, University of Maine, Orono, Maine, USA.
C SullivanDepartment of Molecular and Biomedical Sciences, University of Maine, Orono, Maine, USA Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, Maine, USA.
M F GoodyDepartment of Molecular and Biomedical Sciences, University of Maine, Orono, Maine, USA.
I Rodriguez-NunezDepartment of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA.
J A YoderDepartment of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA.
C H KimDepartment of Molecular and Biomedical Sciences, University of Maine, Orono, Maine, USA Graduate School of Biomedical Sciences and Engineering, University of Maine, Orono, Maine, USA carolkim@maine.edu.
University of Maine · USNorth Carolina State University · US

Funding

Quantitative Biology Research InstituteP20GM103534 · NIGMS · DARTMOUTH COLLEGE · PI AMOS, CHRISTOPHER I. · 2012 to 2016
$8.6M
NIGMS NIH HHS NIH P20GM103534NIGMS NIH HHS P20 GM103534
6 · The paper itself

Abstract

Mitochondria are known primarily as the location of the electron transport chain and energy production in cells. More recently, mitochondria have been shown to be signaling centers for apoptosis and inflammation. Reactive oxygen species (ROS) generated as by-products of the electron transport chain within mitochondria significantly impact cellular signaling pathways. Because of the toxic nature of ROS, mitochondria possess an antioxidant enzyme, superoxide dismutase 2 (SOD2), to neutralize ROS. If mitochondrial antioxidant enzymes are overwhelmed during severe infections, mitochondrial dysfunction can occur and lead to multiorgan failure or death. Pseudomonas aeruginosa is an opportunistic pathogen that can infect immunocompromised patients. Infochemicals and exotoxins associated with P. aeruginosa are capable of causing mitochondrial dysfunction. In this work, we describe the roles of SOD2 and mitochondrial ROS regulation in the zebrafish innate immune response to P. aeruginosa infection. sod2 is upregulated in mammalian macrophages and neutrophils in response to lipopolysaccharide in vitro, and sod2 knockdown in zebrafish results in an increased bacterial burden. Further investigation revealed that phagocyte numbers are compromised in Sod2-deficient zebrafish. Addition of the mitochondrion-targeted ROS-scavenging chemical MitoTEMPO rescues neutrophil numbers and reduces the bacterial burden in Sod2-deficient zebrafish. Our work highlights the importance of mitochondrial ROS regulation by SOD2 in the context of innate immunity and supports the use of mitochondrion-targeted ROS scavengers as potential adjuvant therapies during severe infections.

Indexed as

Immunity, InnateAnimalsLeukocyte CountMacrophagesMitochondriaPseudomonas aeruginosaSuperoxide DismutaseSuperoxide Dismutase 2SuperoxidesZebrafishSuperoxide DismutaseSuperoxide Dismutase 2Superoxides

Identifiers

PMID25385799
PMCPMC4288898
OpenAlexW2115424063

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.