Evidence map›Paper›PMID 30457999›Full record

Observational studyPloS one2018

Augmented concentrations of CX3CL1 are associated with interstitial lung disease in systemic sclerosis.

Anna-Maria Hoffmann-Vold, Stephen Samuel Weigt, Vyacheslav Palchevskiy, Elizabeth Volkmann, Rajan Saggar, Ning Li, Øyvind Midtvedt, May Brit Lund, Torhild Garen, Michael C Fishbein and 8 more

Open access · goldAbstract readMulticenter StudyObservational Study
In one paragraph

Observational study in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 3 pooled it
3.5field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 3 syntheses or guidelines pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Treatable Traits in Systemic Sclerosis.Clinical reviews in allergy & immunology · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Epigenetic Modifications in the Pathogenesis of Systemic Sclerosis.International journal of general medicine · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

18 authors at 2 institutions in 2 countries.

Anna-Maria Hoffmann-VoldDepartment of Rheumatology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.ORCID 0000-0001-6467-7422
Stephen Samuel WeigtDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Vyacheslav PalchevskiyDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Elizabeth VolkmannDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Rajan SaggarDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Ning LiDepartment of Biomathematics, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Øyvind MidtvedtDepartment of Rheumatology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
May Brit LundInstitute of Clinical Medicine, University of Oslo, Rikshospitalet, Oslo, Norway.
Torhild GarenDepartment of Rheumatology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Michael C FishbeinDepartment of Pathology, UCLA, Los Angeles, California, United States of America.
Abbas ArdehaliDepartment of Surgery, UCLA, Los Angeles, California, United States of America.
David J RossDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Thor UelandSection of Clinical Immunology and Infectious Diseases, Oslo University Hospital, Rikshospitalet, Norway.
Pål AukrustSection of Clinical Immunology and Infectious Diseases, Oslo University Hospital, Rikshospitalet, Norway.
Joseph P LynchDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Robert M ElashoffDepartment of Biomathematics, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
Øyvind MolbergDepartment of Rheumatology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
John A BelperioDepartment of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America.
University of California, Los Angeles · USOslo University Hospital · NO

Funding

Role of Surfactant Proteins in Mediating Noninfectious Inflammatory and FibroproP01HL108793 · NHLBI · DUKE UNIVERSITY · PI STRIPP, BARRY R · 2012 to 2022
$21.3M
Immune Mechanisms of AlloinjuryR01HL112990 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BELPERIO, JOHN A · 2012 to 2016
$2.2M
NHLBI NIH HHS P01 HL108793NHLBI NIH HHS R01 HL112990
6 · The paper itself

Abstract

backgroundDysregulation of Fractalkine (CX3CL1) and its receptor CX3CR1 has been linked to the pathobiology of chronic inflammatory conditions. We explored CX3CL1 in systemic sclerosis (SSc) related progressive interstitial lung disease (ILD) and pulmonary hypertension (PH) in two different but complementary sources of biomaterial.

methodsWe collected lung tissue at the time of lung transplantation at UCLA from SSc-ILD patients (n = 12) and healthy donors (n = 12); and serum samples from the prospective Oslo University Hospital SSc cohort (n = 292) and healthy donors (n = 100). CX3CL1 was measured by ELISA. Cellular sources of CX3CL1/CX3CR1 in lung tissues were determined by immunohistochemistry and immunofluorescence. ILD progression and new onset PH endpoints were analysed.

resultsCX3CL1 concentrations were increased in SSc in lung tissue as well as in sera. In the UCLA cohort, CX3CL1 was highly correlated with DLCO. In the SSc-ILD lungs, CX3CL1 was identified in reactive type II pneumocytes and airway epithelial cells. CX3CR1 stained infiltrating interstitial mononuclear cells, especially plasma cells. In the Oslo cohort, CX3CL1 correlated with anti-Topoisomerase-I-antibody and lung fibrosis. CX3CL1 was associated with ILD progression in multivariable regression analysis but not PH.

conclusionCX3CL1 is associated with progressive SSc-ILD but not SSc-PH. The CX3CR1/CX3CL1-biological axis may be involved in recruiting antibody secreting plasma cells to SSc lungs, thereby contributing to the immune-mediated pathobiology of SSc-ILD.

Indexed as

AdultBiomarkersChemokine CX3CL1CX3C Chemokine Receptor 1Disease ProgressionFemaleHumansHypertension, PulmonaryLungLung Diseases, InterstitialLung TransplantationMaleMiddle AgedProspective StudiesRetrospective StudiesScleroderma, SystemicBiomarkersChemokine CX3CL1CX3C Chemokine Receptor 1CX3CL1 protein, humanCX3CR1 protein, humanSDC1 protein, humanSyndecan-1

Identifiers

PMID30457999
PMCPMC6245508
OpenAlexW2901009790

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.