Evidence map›Paper›PMID 16095529›Full record

ArticleRespiratory research2005

A role for MCP-1/CCR2 in interstitial lung disease in children.

Dominik Hartl, Matthias Griese, Thomas Nicolai, Gernot Zissel, Christine Prell, Dietrich Reinhardt, Dolores J Schendel, Susanne Krauss-Etschmann

Open access · goldAbstract readControlled Clinical Trial
In one paragraph

Article in Respiratory research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-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

31 citing papers in PubMed, 60 citations in OpenAlex.

  1. Metoprolol in Critically Ill Patients With COVID-19.Journal of the American College of Cardiology · 2021
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  6. Vistusertib improves pulmonary inflammation and fibrosis by modulating inflammatory/oxidative stress mediators via suppressing the mTOR signalling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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  8. Inflammatory Patterns Associated withPathogens (Basel, Switzerland) · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Obesity and the Development of Lung Fibrosis.Frontiers in pharmacology · 2021
    Review
  15. Review
  16. Article
  17. 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

8 authors at 3 institutions in 1 country.

Dominik HartlChildrens' Hospital, Ludwig-Maximilians-University, Munich, Germany. dominic.hartl@med.uni-muenchen.de
Matthias Griese
Thomas Nicolai
Gernot Zissel
Christine Prell
Dietrich Reinhardt
Dolores J Schendel
Susanne Krauss-Etschmann
Ludwig-Maximilians-Universität München · DEInstitute for Environment and Human Security · DEUniversity Medical Center Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterstitial lung diseases (ILD) are chronic inflammatory disorders leading to pulmonary fibrosis. Monocyte chemotactic protein 1 (MCP-1) promotes collagen synthesis and deletion of the MCP-1 receptor CCR2 protects from pulmonary fibrosis in ILD mouse models. We hypothesized that pulmonary MCP-1 and CCR2+ T cells accumulate in pediatric ILD and are related to disease severity.

methodsBronchoalveolar lavage fluid was obtained from 25 children with ILD and 10 healthy children. Levels of pulmonary MCP-1 and Th1/Th2-associated cytokines were quantified at the protein and the mRNA levels. Pulmonary CCR2+, CCR4+, CCR3+, CCR5+ and CXCR3+ T cells were quantified by flow-cytometry.

resultsCCR2+ T cells and MCP-1 levels were significantly elevated in children with ILD and correlated with forced vital capacity, total lung capacity and ILD disease severity scores. Children with lung fibrosis had significantly higher MCP-1 levels and CCR2+ T cells in bronchoalveolar lavage fluid compared to non-fibrotic children.

conclusionThe results indicate that pulmonary CCR2+ T cells and MCP-1 contribute to the pathogenesis of pediatric ILD and might provide a novel target for therapeutic strategies.

Indexed as

AdolescentAsthmaBronchoalveolar Lavage FluidChemokine CCL2ChildChild, PreschoolFemaleHumansLung Diseases, InterstitialMaleReceptors, CCR2Receptors, ChemokineSeverity of Illness IndexTh1 CellsTh2 CellsCCL2 protein, humanCCR2 protein, humanCcr2 protein, mouseChemokine CCL2Receptors, CCR2Receptors, Chemokine

Identifiers

PMID16095529
PMCPMC1199626
OpenAlexW2130247488

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.