Evidence map›Paper›PMID 26376364›Full record

ArticleMucosal immunology2016

A CCL24-dependent pathway augments eosinophilic airway inflammation in house dust mite-challenged Cd163(-/-) mice.

C Dai, X Yao, E M Gordon, A Barochia, R A Cuento, M Kaler, K S Meyer, K J Keeran, G Z Nugent, K R Jeffries and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. CD163Basic research in cardiology · 2025
    Article
  7. IL-1β and iNOS can drive the asthmatic comorbidities and decrease of lung function in perennial allergic rhinitis children.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2024
    Article
  8. Review
  9. Neuroinflammation in Obese Children.Bulletin of experimental biology and medicine · 2024
    Article
  10. Article
  11. Article
  12. Targeting of CD163International journal of molecular sciences · 2020
    Review
  13. Systemic corticosteroid therapy augmentsPostepy dermatologii i alergologii · 2020
    Article
  14. The different faces of the macrophage in asthma.Current opinion in pulmonary medicine · 2020
    Review
  15. Article
  16. Serum IL-1β can be a biomarker in children with severe persistent allergic rhinitis.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019
    Article
  17. Article
  18. Article
  19. Article
  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

17 authors at 2 institutions in 1 country.

C DaiLaboratory of Asthma and Lung Inflammation, NHLBI, NIH, Bethesda, Maryland, USA.
X YaoLaboratory of Asthma and Lung Inflammation, NHLBI, NIH, Bethesda, Maryland, USA.
E M GordonLaboratory of Asthma and Lung Inflammation, NHLBI, NIH, Bethesda, Maryland, USA.
A BarochiaLaboratory of Asthma and Lung Inflammation, NHLBI, NIH, Bethesda, Maryland, USA.
R A CuentoLaboratory of Asthma and Lung Inflammation, NHLBI, NIH, Bethesda, Maryland, USA.
M KalerLaboratory of Asthma and Lung Inflammation, NHLBI, NIH, Bethesda, Maryland, USA.
K S MeyerLaboratory of Asthma and Lung Inflammation, NHLBI, NIH, Bethesda, Maryland, USA.
K J KeeranAnimal Surgery and Resources Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
G Z NugentAnimal Surgery and Resources Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
K R JeffriesAnimal Surgery and Resources Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
X QuPathology Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
Z-X YuPathology Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
A AponteProteomics Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
M GucekProteomics Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
P K DagurFlow Cytometry Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
J P McCoyFlow Cytometry Core Facility, NHLBI, NIH, Bethesda, Maryland, USA.
S J LevineLaboratory of Asthma and Lung Inflammation, NHLBI, NIH, Bethesda, Maryland, USA.
National Institutes of Health · USNational Heart Lung and Blood Institute · US

Funding

NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
Flow Cytometry Core FacilityZICHL005905 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI DAGUR, PRADEEP · 2009 to 2025
$32.3M
Proteomics CoreZICHL005903 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI GUCEK, MARJAN · 2009 to 2022
$23.3M
Fiberoptic Bronchoscopy in Patients with AsthmaZIAHL006197 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LEVINE, STEWART · 2015 to 2024
$14.8M
Mechanisms of Asthma Pathogenesis and TreatmentZIAHL002548 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LEVINE, STEWART · 2009 to 2017
$4.7M
Intramural NIH HHS ZIA HL002548
6 · The paper itself

Abstract

CD163 is a macrophage scavenger receptor with anti-inflammatory and pro-inflammatory functions. Here, we report that alveolar macrophages (AMΦs) from asthmatic subjects had reduced cell-surface expression of CD163, which suggested that CD163 might modulate the pathogenesis of asthma. Consistent with this, house dust mite (HDM)-challenged Cd163(-/-) mice displayed increases in airway eosinophils and mucous cell metaplasia (MCM). The increased airway eosinophils and MCM in HDM-challenged Cd163(-/-) mice were mediated by augmented CCL24 production and could be reversed by administration of a neutralizing anti-CCL24 antibody. A proteomic analysis identified the calcium-dependent binding of CD163 to Dermatophagoides pteronyssinus peptidase 1 (Der p1). Der p1-challenged Cd163(-/-) mice had the same phenotype as HDM-challenged Cd163(-/-) mice with increases in airway eosinophils, MCM and CCL24 production, while Der p1 induced CCL24 secretion by bone marrow-derived macrophages (BMMΦs) from Cd163(-/-) mice, but not BMMΦs from wild-type (WT) mice. Finally, airway eosinophils and bronchoalveolar lavage fluid CCL24 levels were increased in Der p1-challenged WT mice that received adoptively transferred AMΦ's from Cd163(-/-) mice. Thus, we have identified CD163 as a macrophage receptor that binds Der p1. Furthermore, we have shown that HDM-challenged Cd163(-/-) mice have increased eosinophilic airway inflammation and MCM that are mediated by a CCL24-dependent mechanism.

Indexed as

AnimalsAntibodies, NeutralizingAntigens, CDAntigens, DermatophagoidesAntigens, Differentiation, MyelomonocyticArthropod ProteinsAsthmaCD163 AntigenCell MovementCells, CulturedChemokine CCL24Cysteine EndopeptidasesEosinophilsHumansMacrophages, AlveolarMetaplasiaAntibodies, NeutralizingAntigens, CDAntigens, DermatophagoidesAntigens, Differentiation, MyelomonocyticArthropod ProteinsCD163 AntigenChemokine CCL24Cysteine EndopeptidasesDermatophagoides pteronyssinus antigen p 1Receptors, Cell Surface

Identifiers

PMID26376364
PMCPMC4794428
OpenAlexW2345045963

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.