Evidence map›Paper›PMID 20870892›Full record

ArticleAmerican journal of respiratory cell and molecular biology2011

The chemokine, CCL3, and its receptor, CCR1, mediate thoracic radiation-induced pulmonary fibrosis.

Xuebin Yang, William Walton, Donald N Cook, Xiaoyang Hua, Stephen Tilley, Christopher A Haskell, Richard Horuk, A William Blackstock, Suzanne L Kirby

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.6field-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

35 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Observational
  8. Review
  9. Article
  10. Influence of the irradiated pulmonary microenvironment on macrophage and T cell dynamics.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023
    Article
  11. Article
  12. The roles of CC chemokines in response to radiation.Radiation oncology (London, England) · 2022
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Cryptotanshinone Ameliorates Radiation-Induced Lung Injury in Rats.Evidence-based complementary and alternative medicine : eCAM · 2019
    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

9 authors at 5 institutions in 1 country.

Xuebin YangDepartment of Pathology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
William Walton
Donald N Cook
Xiaoyang Hua
Stephen Tilley
Christopher A Haskell
Richard Horuk
A William Blackstock
Suzanne L Kirby
University of North Carolina at Chapel Hill · USBayer (United States) · USNational Institutes of Health · USUniversity of California, Davis · USWake Forest University · US

Funding

Somatostatin analogues as countermeasures against intestinal radiation toxicityU19AI067798 · NIAID · DUKE UNIVERSITY · PI DOAN, PHUONG LINH · 2005 to 2024
$82.1M
Allergic sensitization through the airwayZIAES102025 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI COOK, DONALD N · 2009 to 2025
$32.6M
Chemokines in Radiation Induced Pulmonary FibrosisR01CA098641 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KIRBY, SUZANNE L · 2004 to 2007
$940k
NCI NIH HHS 5R0 1CA098641-02NIAID NIH HHS 5-U19-AI067798
6 · The paper itself

Abstract

Patients receiving thoracic radiation often develop pulmonary injury and fibrosis. Currently, there are no effective measures to prevent or treat these conditions. We tested whether blockade of the chemokine, CC chemokine ligand (CCL) 3, and its receptors, CC chemokine receptor (CCR) 1 and CCR5, can prevent radiation-induced lung inflammation and fibrosis. C57BL/6J mice received thoracic radiation, and the interaction of CCL3 with CCR1 or CCR5 was blocked using genetic techniques, or by pharmacologic intervention. Lung inflammation was assessed by histochemical staining of lung tissue and by flow cytometry. Fibrosis was measured by hydroxyproline assays and collagen staining, and lung function was studied by invasive procedures. Irradiated mice lacking CCL3 or its receptor, CCR1, did not develop the lung inflammation, fibrosis, and decline in lung function seen in irradiated wild-type mice. Pharmacologic treatment of wild-type mice with a small molecule inhibitor of CCR1 also prevented lung inflammation and fibrosis. By contrast, mice lacking CCR5 were not protected from radiation-induced injury and fibrosis. The selective interaction of CCL3 with its receptor, CCR1, is critical for radiation-induced lung inflammation and fibrosis, and these conditions can be largely prevented by a small molecule inhibitor of CCR1.

Indexed as

AnimalsChemokine CCL3Gamma RaysHydroxyprolineLungMiceMice, KnockoutPhenylurea CompoundsPiperidinesRadiation Injuries, ExperimentalRadiation PneumonitisReceptors, CCR1Receptors, CCR5BX 471Ccl3 protein, mouseCcr1 protein, mouseChemokine CCL3HydroxyprolinePhenylurea CompoundsPiperidinesReceptors, CCR1Receptors, CCR5

Identifiers

PMID20870892
PMCPMC3145066
OpenAlexW2001682159

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.