Evidence map›Paper›PMID 35367162›Full record

ArticleJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society2022

Club cell secretory protein and lung function in children with cystic fibrosis.

Jing Zhai, Mary J Emond, Amber Spangenberg, Debra A Stern, Monica M Vasquez, Elizabeth E Blue, Kati J Buckingham, Duane L Sherrill, Marilyn Halonen, Ronald L Gibson and 5 more

Open access · greenAbstract read
In one paragraph

Article in Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Observational
  2. Article
  3. Article
  4. Review
  5. Article
  6. Frontiers in immunology · 2025
    Article
  7. Review
  8. Article
  9. Review
  10. Circulating biomarkers of airflow limitation across the life span.The Journal of allergy and clinical immunology · 2024
    Article
  11. Article
  12. Article
  13. CC16: A Treatable Trait in Asthma?American journal of respiratory and critical care medicine · 2023
    Article
  14. Article
  15. Low CC16 mRNA Expression Levels in Bronchial Epithelial Cells Are Associated with Asthma Severity.American journal of respiratory and critical care medicine · 2023
    Article
  16. Review
  17. Article
  18. 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

15 authors at 4 institutions in 1 country.

Jing ZhaiAsthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States.
Mary J EmondDepartment of Biostatistics, University of Washington, Seattle, WA, United States.
Amber SpangenbergAsthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States.
Debra A SternAsthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States.
Monica M VasquezAsthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States.
Elizabeth E BlueDivision of Medical Genetics, Department of Medicine, University of Washington, Seattle, WA, United States; Brotman-Baty Institute for Precision Medicine, Seattle, WA, United States.
Kati J BuckinghamDivision of Genetic Medicine, Department of Pediatrics, University of Washington, Seattle, WA, United States.
Duane L SherrillAsthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States.
Marilyn HalonenAsthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States.
Ronald L GibsonDepartment of Pediatrics, University of Washington School of Medicine, Seattle, WA, United States.
Margaret RosenfeldDepartment of Pediatrics, University of Washington School of Medicine, Seattle, WA, United States.
Scott D SagelDepartment of Pediatrics, Children's Hospital Colorado and University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Michael J BamshadBrotman-Baty Institute for Precision Medicine, Seattle, WA, United States; Division of Genetic Medicine, Department of Pediatrics, University of Washington, Seattle, WA, United States; Department of Genome Sciences, University of Washington, Seattle, WA, United States.
Wayne J MorganAsthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States; Department of Pediatrics, University of Arizona, Tucson, AZ, United States. Electronic address: wjmorgan@email.arizona.edu.
Stefano GuerraAsthma and Airway Disease Research Center, University of Arizona, Tucson, AZ, United States; Department of Medicine, University of Arizona, Tucson, AZ, United States. Electronic address: stefano@email.arizona.edu.
University of Arizona · USUniversity of Washington · USChildren's Hospital Colorado · USUniversity of Washington Medical Center · US

Funding

NIH Prior Approval Process ProfessionalUL1TR002535 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2018 to 2022
$51.1M
Translational Research Center to Expedite Novel Therapies in Cystic FibrosisP30DK089507 · NIDDK · SEATTLE CHILDREN'S HOSPITAL · PI Christopher Hooper Goss · 2010 to 2026
$21.4M
CC16 in Childhood and Resilience to Persistent Asthma into Adult Life (Supplement)R01AI135108 · NIAID · UNIVERSITY OF ARIZONA · PI Stefano Guerra · 2017 to 2026
$5.4M
NCATS NIH HHS UL1 TR002535NIAID NIH HHS R01 AI135108NIDDK NIH HHS P30 DK089507
6 · The paper itself

Abstract

backgroundClub cell secretory protein (CC16) exerts anti-inflammatory functions in lung disease. We sought to determine the relation of serum CC16 deficits and genetic variants that control serum CC16 to lung function among children with cystic fibrosis (CF).

methodsWe used longitudinal data from CF children (EPIC Study) with no positive cultures for Pseudomonas aeruginosa prior to enrollment. Circulating levels of CC16 and an inflammatory score (generated from CRP, SAA, calprotectin, G-CSF) were compared between participants with the lowest and highest FEV

resultsCompared with the HLF group, the LLF group had lower levels of CC16 (geometric means: 8.2 vs 6.5 ng/ml, respectively; p = 0.0002) and higher levels of the normalized inflammatory score (-0.21 vs 0.21, p = 0.0007). Participants in the lowest CC16 and highest inflammation tertile had the highest odds for having LLF (p<0.0001 for comparison with participants in the highest CC16 and lowest inflammation tertile). Among seven SNVs associated with circulating CC16, the top SNV rs3741240 was associated with decline of FEV

conclusionsSerum CC16 deficits are strongly associated with severity of CF lung disease and their effects are additive with systemic inflammation. The rs3741240 A allele is associated with low circulating CC16 and, possibly, accelerated lung function decline in CF.

Indexed as

Cystic FibrosisUteroglobinAdolescentChildGranulocyte Colony-Stimulating FactorHumansInflammationLeukocyte L1 Antigen ComplexLungNucleotidesGranulocyte Colony-Stimulating FactorLeukocyte L1 Antigen ComplexNucleotidesUteroglobinClub cell secretory proteinCystic fibrosisLung function

Identifiers

PMID35367162
PMCPMC9509401
OpenAlexW4221095497

What OpenQuestion holds

Textmetadata
LicenceTDM
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.