Evidence map›Paper›PMID 17898169›Full record

Trial reportProceedings of the National Academy of Sciences of the United States of America2007

Genome-wide profiling identifies epithelial cell genes associated with asthma and with treatment response to corticosteroids.

Prescott G Woodruff, Homer A Boushey, Gregory M Dolganov, Chris S Barker, Yee Hwa Yang, Samantha Donnelly, Almut Ellwanger, Sukhvinder S Sidhu, Trang P Dao-Pick, Carlos Pantoja and 3 more

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 409 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
409citing papers in PubMed, 4 pooled it
11.5field-weighted citation impact, top 1% 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

409 citing papers in PubMed, 4 syntheses or guidelines pooled it, 830 citations in OpenAlex.

  1. Sex-biased Gene Expression Underlies Immune Dysfunction in Asthma.American journal of respiratory cell and molecular biology · 2025
    Pooled it
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  6. Dexamethasone-Induced FKBP51 Expression in CD4Frontiers in immunology · 2021
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349 more citing papers are in PubMed but not listed here.

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

13 authors at 6 institutions in 3 countries.

Prescott G WoodruffDivision of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, San Francisco, CA 94143, USA.
Homer A Boushey
Gregory M Dolganov
Chris S Barker
Yee Hwa Yang
Samantha Donnelly
Almut Ellwanger
Sukhvinder S Sidhu
Trang P Dao-Pick
Carlos Pantoja
David J Erle
Keith R Yamamoto
John V Fahy
Cardiovascular Institute Hospital · JPPulmonary and Critical Care Associates · USUniversity of California, San Francisco · USGladstone Institutes · USStanford University · USUniversity of Sydney · AU

Funding

ZD1839 FOR MALIGNANT ASTROCYTOMA OR GLIOBLASTOMA AND MENINGIOMAM01RR000079 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KESSLER, DAVID A · 1985 to 2006
$26.0M
WELFARE REFORM AND THE PERINATAL HEALTH OF IMMIGRANTSM01RR000083 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KESSLER, DAVID A · 1985 to 2006
$21.1M
ROLE OF SELECTINS IN LEUKOCYTE RECRUITMENT TO INFLAMED AIRWAYS IN ASTHMAP50HL056385 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI SHEPPARD, DEAN · 1996 to 2005
$10.5M
Protein carbohydrate interactions in the pathophysiology of asthma exacerbationsR01HL080414 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI John V Fahy · 2005 to 2026
$9.2M
GENE REGULATION BY STEROID RECEPTOR PROTEINSR01CA020535 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI YAMAMOTO, KEITH ROBERT · 1985 to 2018
$8.9M
Shared Microarray FacilityR01HL072301 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI ERLE, DAVID J · 2002 to 2005
$2.7M
Airway Epithelial Responses to Allergic InflammationR01HL085089 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ERLE, DAVID J · 2006 to 2010
$1.9M
T CELL INFLAMMATION AND MUCIN HYPERSECRETION IN COPDR01HL066564 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI FAHY, JOHN V · 2001 to 2004
$1.3M
MECHANISMS OF SMOOTH MUSCLE HYPERREACTIVITY ON ASTHMAK23RR017002 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WOODRUFF, PRESCOTT G · 2002 to 2006
$744k
GENE REGULATION BY STEROID RECEPTOR PROTEINSR37CA020535 · NCI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI YAMAMOTO, KEITH ROBERT · 1990 to 1998
–
NCI NIH HHS CA020535NCI NIH HHS R01 CA020535NCI NIH HHS R37 CA020535NCRR NIH HHS K23 RR017002NCRR NIH HHS M01 RR000079NCRR NIH HHS M01 RR000083NCRR NIH HHS RR00079NCRR NIH HHS RR00083NCRR NIH HHS RR17002NHLBI NIH HHS HL080414NHLBI NIH HHS HL5683NHLBI NIH HHS HL66564NHLBI NIH HHS HL72301NHLBI NIH HHS P50 HL056385NHLBI NIH HHS R01 HL066564NHLBI NIH HHS R01 HL072301NHLBI NIH HHS R01 HL080414NHLBI NIH HHS R01 HL085089
6 · The paper itself

Abstract

Airway inflammation and epithelial remodeling are two key features of asthma. IL-13 and other cytokines produced during T helper type 2 cell-driven allergic inflammation contribute to airway epithelial goblet cell metaplasia and may alter epithelial-mesenchymal signaling, leading to increased subepithelial fibrosis or hyperplasia of smooth muscle. The beneficial effects of corticosteroids in asthma could relate to their ability to directly or indirectly decrease epithelial cell activation by inflammatory cells and cytokines. To identify markers of epithelial cell dysfunction and the effects of corticosteroids on epithelial cells in asthma, we studied airway epithelial cells collected from asthmatic subjects enrolled in a randomized controlled trial of inhaled corticosteroids, from healthy subjects and from smokers (disease control). By using gene expression microarrays, we found that chloride channel, calcium-activated, family member 1 (CLCA1), periostin, and serine peptidase inhibitor, clade B (ovalbumin), member 2 (serpinB2) were up-regulated in asthma but not in smokers. Corticosteroid treatment down-regulated expression of these three genes and markedly up-regulated expression of FK506-binding protein 51 (FKBP51). Whereas high baseline expression of CLCA1, periostin, and serpinB2 was associated with a good clinical response to corticosteroids, high expression of FKBP51 was associated with a poor response. By using airway epithelial cells in culture, we found that IL-13 increased expression of CLCA1, periostin, and serpinB2, an effect that was suppressed by corticosteroids. Corticosteroids also induced expression of FKBP51. Taken together, our findings show that airway epithelial cells in asthma have a distinct activation profile and identify direct and cell-autonomous effects of corticosteroid treatment on airway epithelial cells that relate to treatment responses and can now be the focus of specific mechanistic studies.

Indexed as

Gene Expression ProfilingGenome, HumanAdministration, InhalationAdrenal Cortex HormonesAsthmaBronchoscopyCell Adhesion MoleculesChloride ChannelsEpithelial CellsHumansHypersensitivityInflammationOligonucleotide Array Sequence AnalysisReference ValuesSerpinsSmokingAdrenal Cortex HormonesCell Adhesion MoleculesChloride ChannelsCLCA1 protein, humanPOSTN protein, humanserpin-2Serpins

Identifiers

PMID17898169
PMCPMC2000427
OpenAlexW2164092307

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.