Evidence map›Paper›PMID 15681819›Full record

ArticleThe American journal of pathology2005

Temporal production of CCL28 corresponds to eosinophil accumulation and airway hyperreactivity in allergic airway inflammation.

Alison E John, Molly S Thomas, Aaron A Berlin, Nicholas W Lukacs

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. The Role of Atopy in COPD and Asthma.Frontiers in medicine · 2021
    Review
  8. Review
  9. Eosinophilic Vasculitis.Current rheumatology reports · 2020
    Review
  10. Article
  11. Article
  12. CCL28 Is Involved in Mucosal IgA Responses, Olfaction, and Resistance to Enteric Infections.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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  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

4 authors at 1 institution in 1 country.

Alison E JohnDepartment of Pathology, University of Michigan Medical School, 1301 Catherine Road, Ann Arbor MI 48109-0602, USA.
Molly S Thomas
Aaron A Berlin
Nicholas W Lukacs
University of Michigan–Ann Arbor · US

Funding

The Role of C-C Chemokines in Eosinophil Airway InflammationR01AI036302 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 2001 to 2018
$5.6M
C-C CHEMOKINES AND EOSINOPHIL AIRWAY INFLAMMATIONR29AI036302 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUKACS, NICHOLAS W · 1996 to 2000
$107k
NHLBI NIH HHS HL 3196NIAID NIH HHS AI 36302NIAID NIH HHS R01 AI036302NIAID NIH HHS R29 AI036302
6 · The paper itself

Abstract

CCL28 is a recently identified chemokine ligand for CCR10 and CCR3 that has been identified in mucosal epithelial surfaces in diverse tissues. CCL28-mediated eosinophil chemotaxis and peroxidase release were inhibited by preincubation of cells with anti-CCR3. CCL28 was constitutively expressed in lung tissue collected from nonsensitized control mice but increased levels were found in mice sensitized and rechallenged with cockroach antigen (CRA). CCL28 levels peaked in the lungs 24 hours after intratracheal challenge with CRA, whereas eotaxin expression peaked at 8 hours. Increased expression of CCR3 but not CCR10 could be detected during the induction of the CRA-induced pulmonary inflammation. To investigate the role of CCL28 in allergic airway responses, mice were treated with CCL28 antiserum 1 hour before receiving the final CRA challenge. The level of airway hyperresponsiveness in mice treated with anti-CCL28 was significantly reduced at 24 hours, but not 8 hours, compared to mice receiving control serum. This reduction was not related to decreased Th2 cytokine, chemokine, or leukotriene levels at 24 hours although peribronchial eosinophilia was significantly reduced. Thus, CCL28 appears to play a role in regulating eosinophil recruitment to peribronchial regions of the lung possibly by coordinated temporal production with eotaxin.

Indexed as

AnimalsBronchial HyperreactivityChemokine CCL11ChemokinesChemokines, CCChemotaxisDose-Response Relationship, DrugEnzyme-Linked Immunosorbent AssayEosinophilsGene Expression RegulationImmunohistochemistryInflammationLeukotriene C4LeukotrienesLigandsLungCCL11 protein, humanCcl11 protein, mouseCCL28 protein, humanCCR10 protein, humanCcr10 protein, mouseCCR3 protein, humanCcr3 protein, mouseChemokine CCL11ChemokinesChemokines, CCLeukotriene C4LeukotrienesLigandsPeroxidasesReceptors, CCR10Receptors, CCR3Receptors, ChemokineRNA

Identifiers

PMID15681819
PMCPMC1602329
OpenAlexW2165539495

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.