Evidence map›Paper›PMID 23637937›Full record

ArticlePloS one2013

Role of arginase 1 from myeloid cells in th2-dominated lung inflammation.

Luke Barron, Amber M Smith, Karim C El Kasmi, Joseph E Qualls, Xiaozhu Huang, Allen Cheever, Lee A Borthwick, Mark S Wilson, Peter J Murray, Thomas A Wynn

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Dissecting inflammation in the immunemetabolomic era.Cellular and molecular life sciences : CMLS · 2025
    Review
  3. The roles of arginases and arginine in immunity.Nature reviews. Immunology · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Arginine-dependent immune responses.Cellular and molecular life sciences : CMLS · 2021
    Review
  18. Review
  19. Arginine Therapy for Lung Diseases.Frontiers in pharmacology · 2021
    Review
  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

10 authors at 5 institutions in 2 countries.

Luke BarronProgram in Barrier Immunity and Repair, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America. BarronL@niaid.nih.gov
Amber M Smith
Karim C El Kasmi
Joseph E Qualls
Xiaozhu Huang
Allen Cheever
Lee A Borthwick
Mark S Wilson
Peter J Murray
Thomas A Wynn
St. Jude Children's Research Hospital · USNational Institutes of Health · USBiomedical Research Institute · USNewcastle University · GBUniversity of California, San Francisco · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Approaches To Immunological Intervention In SchistosomiasisZIAAI000829 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI WYNN, THOMAS · 2009 to 2018
$9.9M
Role of Macrophage Arginase in Anti-Bacterial ImmunityR01AI062921 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI MURRAY, PETER J. · 2005 to 2009
$1.3M
Medical Research Council MC_UP_A253_1028NCI NIH HHS P30 CA021765NCI NIH HHS P30 CA21765NIAID NIH HHS AI062921NIAID NIH HHS R01 AI062921
6 · The paper itself

Abstract

Th2-driven lung inflammation increases Arginase 1 (Arg1) expression in alternatively-activated macrophages (AAMs). AAMs modulate T cell and wound healing responses and Arg1 might contribute to asthma pathogenesis by inhibiting nitric oxide production, regulating fibrosis, modulating arginine metabolism and restricting T cell proliferation. We used mice lacking Arg1 in myeloid cells to investigate the contribution of Arg1 to lung inflammation and pathophysiology. In six model systems encompassing acute and chronic Th2-mediated lung inflammation we observed neither a pathogenic nor protective role for myeloid-expressed Arg1. The number and composition of inflammatory cells in the airways and lungs, mucus secretion, collagen deposition, airway hyper-responsiveness, and T cell cytokine production were not altered if AAMs were deficient in Arg1 or simultaneously in both Arg1 and NOS2. Our results argue that Arg1 is a general feature of alternative activation but only selectively regulates Th2 responses. Therefore, attempts to experimentally or therapeutically inhibit arginase activity in the lung should be examined with caution.

Indexed as

AnimalsAntigens, HelminthArginaseAspergillusGene ExpressionGranulomaMacrophage ActivationMacrophagesMiceMice, KnockoutMyeloid CellsOvalbuminPneumoniaSchistosoma mansoniTh2 CellsAntigens, HelminthArg1 protein, mouseArginaseOvalbumin

Identifiers

PMID23637937
PMCPMC3634833
OpenAlexW1994718754

What OpenQuestion holds

Textmetadata
LicenceCC0
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.