Evidence map›Paper›PMID 23484005›Full record

ArticlePloS one2013

A novel anti-inflammatory and pro-resolving role for resolvin D1 in acute cigarette smoke-induced lung inflammation.

Hsi-Min Hsiao, Ramil E Sapinoro, Thomas H Thatcher, Amanda Croasdell, Elizabeth P Levy, Robert A Fulton, Keith C Olsen, Stephen J Pollock, Charles N Serhan, Richard P Phipps and 1 more

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 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
17.6field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 207 citations in OpenAlex.

  1. Altered tissue specialized pro-resolving mediators in chronic rhinosinusitis.Prostaglandins, leukotrienes, and essential fatty acids · 2021
    Trial
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  8. Linking Lipid Metabolism and Immune Function: New Insights into Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  9. Review
  10. Article
  11. SiOScientific reports · 2025
    Article
  12. Article
  13. Efferocytosis in Homeostasis.Advances in experimental medicine and biology · 2025
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Inhaled toxicants and pulmonary lipid metabolism: biological consequences and therapeutic interventions.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article

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

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

11 authors at 2 institutions in 1 country.

Hsi-Min HsiaoDepartment of Pathology and Laboratory Medicine, University of Rochester, Rochester, New York, USA.
Ramil E Sapinoro
Thomas H Thatcher
Amanda Croasdell
Elizabeth P Levy
Robert A Fulton
Keith C Olsen
Stephen J Pollock
Charles N Serhan
Richard P Phipps
Patricia J Sime
University of Rochester · USHarvard University · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI B Paige Lawrence · 1985 to 2026
$42.8M
UNIVERSITY OF ROCHESTER'S RESEARCH ASSOCIATE ORGANIZATIONUL1RR024160 · NCRR · UNIVERSITY OF ROCHESTER · PI PEARSON, THOMAS ARTHUR · 2006 to 2011
$38.7M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
The University of Rochester's Clinical and Translational Science InstituteUL1TR000042 · NCATS · UNIVERSITY OF ROCHESTER · PI BENNETT, NANCY M, KIEBURTZ, KARL D. · 2012 to 2015
$14.4M
MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL066988 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE N, O'REILLY, MICHAEL A · 2001 to 2021
$8.1M
Role of the Aryl Hydrocarbon Receptor in Lung InflammationR01HL088325 · NHLBI · UNIVERSITY OF ROCHESTER · PI SIME, PATRICIA JANET · 2008 to 2012
$1.9M
BCL-2, ROS, AND CELL DEATH IN DEVELOPMENTAL TOXICITYR01ES007026 · NIEHS · UNIVERSITY OF WASHINGTON · PI MIRKES, PHILIP E · 1996 to 2002
$1.2M
NCATS NIH HHS 8UL1TR000042NCATS NIH HHS UL1 TR000042NCRR NIH HHS UL1 RR024160NHLBI NIH HHS HL088325-02S1NHLBI NIH HHS HL66988NHLBI NIH HHS R01 HL088325NHLBI NIH HHS T32 HL066988NIEHS NIH HHS ES01247NIEHS NIH HHS ES07026NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R01 ES007026NIEHS NIH HHS T32 ES007026
6 · The paper itself

Abstract

introductionCigarette smoke is a profound pro-inflammatory stimulus that contributes to acute lung injuries and to chronic lung disease including COPD (emphysema and chronic bronchitis). Until recently, it was assumed that resolution of inflammation was a passive process that occurred once the inflammatory stimulus was removed. It is now recognized that resolution of inflammation is a bioactive process, mediated by specialized lipid mediators, and that normal homeostasis is maintained by a balance between pro-inflammatory and pro-resolving pathways. These novel small lipid mediators, including the resolvins, protectins and maresins, are bioactive products mainly derived from dietary omega-3 and omega-6 polyunsaturated fatty acids (PUFA). We hypothesize that resolvin D1 (RvD1) has potent anti-inflammatory and pro-resolving effects in a model of cigarette smoke-induced lung inflammation.

methodsPrimary human lung fibroblasts, small airway epithelial cells and blood monocytes were treated with IL-1β or cigarette smoke extract in combination with RvD1 in vitro, production of pro-inflammatory mediators was measured. Mice were exposed to dilute mainstream cigarette smoke and treated with RvD1 either concurrently with smoke or after smoking cessation. The effects on lung inflammation and lung macrophage populations were assessed.

resultsRvD1 suppressed production of pro-inflammatory mediators by primary human cells in a dose-dependent manner. Treatment of mice with RvD1 concurrently with cigarette smoke exposure significantly reduced neutrophilic lung inflammation and production of pro-inflammatory cytokines, while upregulating the anti-inflammatory cytokine IL-10. RvD1 promoted differentiation of alternatively activated (M2) macrophages and neutrophil efferocytosis. RvD1 also accelerated the resolution of lung inflammation when given after the final smoke exposure.

conclusionsRvD1 has potent anti-inflammatory and pro-resolving effects in cells and mice exposed to cigarette smoke. Resolvins have strong potential as a novel therapeutic approach to resolve lung injury caused by smoke and pulmonary toxicants.

Indexed as

Analysis of VarianceAnimalsBronchoalveolar Lavage FluidChemokinesCytokinesDNA PrimersDocosahexaenoic AcidsFemaleFibroblastsHomeostasisHumansLungMiceMice, Inbred C57BLPhagocytosisPneumoniaChemokinesCytokinesDNA PrimersDocosahexaenoic Acidsresolvin D1

Identifiers

PMID23484005
PMCPMC3590122
OpenAlexW2169973614

What OpenQuestion holds

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Registered trials

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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.