Evidence map›Paper›PMID 23002442›Full record

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

A serpinB1 regulatory mechanism is essential for restricting neutrophil extracellular trap generation.

Kalamo Farley, J Michael Stolley, Picheng Zhao, Jessica Cooley, Eileen Remold-O'Donnell

Abstract read
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 59 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 8% 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

59 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Taurine inhibitsFrontiers in immunology · 2022
    Article
  17. Serine protease inhibitor derived fromFrontiers in cellular and infection microbiology · 2022
    Article
  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

5 authors at 2 institutions in 1 country.

Kalamo FarleyImmune Disease Institute, Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, USA.
J Michael Stolley
Picheng Zhao
Jessica Cooley
Eileen Remold-O'Donnell
Boston Children's Hospital · USHarvard University · US

Funding

ROLE OF PROTEASE IN INFECTION &INFLAMMATION OF COPDR01HL066548 · NHLBI · IMMUNE DISEASE INSTITUTE, INC. · PI REMOLD-O'DONNELL, EILEEN · 2000 to 2010
$3.7M
SERPINB1/MNEI: Role in innate immune defense against influenza virus infectionR21AI072552 · NIAID · IMMUNE DISEASE INSTITUTE, INC. · PI REMOLD-O'DONNELL, EILEEN · 2007 to 2008
$516k
Regulation of NETosis in antibacterial lung defenseR21AI103407 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI REMOLD-O'DONNELL, EILEEN · 2013 to 2014
$482k
NHLBI NIH HHS HL-066548NHLBI NIH HHS R01 HL066548NIAID NIH HHS AI-072552NIAID NIH HHS R21 AI072552NIAID NIH HHS R21 AI103407
6 · The paper itself

Abstract

NETosis (neutrophil extracellular trap [NET] generation), a programmed death pathway initiated in mature neutrophils by pathogens and inflammatory mediators, can be a protective process that sequesters microbes and prevents spread of infection, but it can also be a pathological process that causes inflammation and serious tissue injury. Little is known about the regulatory mechanism. Previously, we demonstrated that serpinb1-deficient mice are highly susceptible to pulmonary bacterial and viral infections due to inflammation and tissue injury associated with increased neutrophilic death. In this study, we used in vitro and in vivo approaches to investigate whether SerpinB1 regulates NETosis. We found that serpinb1-deficient bone marrow and lung neutrophils are hypersusceptible to NETosis induced by multiple mediators in both an NADPH-dependent and -independent manner, indicating a deeply rooted regulatory role in NETosis. This role is further supported by increased nuclear expansion (representing chromatin decondensation) of PMA-treated serpinb1-deficient neutrophils compared with wild-type, by migration of SerpinB1 from the cytoplasm to the nucleus of human neutrophils that is coincident with or preceding early conversion of lobulated (segmented) nuclei to delobulated (spherical) morphology, as well as by the finding that exogenous human recombinant SerpinB1 abrogates NET production. NETosis of serpinb1-deficient neutrophils is also increased in vivo during Pseudomonas aeruginosa lung infection. The findings identify a previously unrecognized regulatory mechanism involving SerpinB1 that restricts the production of NETs.

Indexed as

AnimalsBone Marrow CellsCell DeathCell NucleusCells, CulturedCytoplasmExtracellular FluidFemaleGenetic Predisposition to DiseaseHumansMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutNeutrophilsPneumonia, BacterialSerpinb1a protein, mouseSerpins

Identifiers

PMID23002442
PMCPMC3964884
OpenAlexW2108210127

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.