Evidence map›Paper›PMID 26729801›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2016

Molecular Mechanisms of Airway Hyperresponsiveness in a Murine Model of Steroid-Resistant Airway Inflammation.

Michelle L Manni, Sivanarayana Mandalapu, Kevin J McHugh, M Merle Elloso, Paul L Dudas, John F Alcorn

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Dog allergen-induced asthma in mice: a relevant model of T2Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. T helper 2 cells in asthma.The Journal of experimental medicine · 2023
    Review
  9. Article
  10. Review
  11. TThe Journal of allergy and clinical immunology · 2022
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. MethylatedBiology open · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Michelle L ManniDepartment of Pediatrics, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, Pittsburgh, PA 15224; and.
Sivanarayana MandalapuDepartment of Pediatrics, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, Pittsburgh, PA 15224; and.
Kevin J McHughDepartment of Pediatrics, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, Pittsburgh, PA 15224; and.
M Merle EllosoJanssen Research & Development, LLC, Spring House, PA 19477.
Paul L DudasJanssen Research & Development, LLC, Spring House, PA 19477.
John F AlcornDepartment of Pediatrics, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, Pittsburgh, PA 15224; and john.alcorn@chp.edu.
Children's Hospital of Pittsburgh · USJanssen (United States) · USUniversity of Pittsburgh Medical Center · US

Funding

Influenza A Inhibits TH17 Host Defense Against Bacterial PneumoniaR01HL107380 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ALCORN, JOHN F · 2012 to 2024
$5.4M
NHLBI NIH HHS R01 HL107380
6 · The paper itself

Abstract

IL-13 and IL-17A, produced mainly by Th2 and Th17 cells, respectively, have an influential role in asthma pathogenesis. We examined the role of IL-13 and IL-17A in mediating airway hyperresponsiveness (AHR), lung inflammation, and mucus metaplasia in a dual Th2/Th17 model of asthma. IL-13 and/or IL-17A were neutralized using mAbs. Th2/Th17 adoptive transfer induced a mixed asthma phenotype characterized by elevated eosinophilia and neutrophilia, tissue inflammation, mucus metaplasia, and AHR that were partially reversible with steroid treatment. Pulmonary inflammation and quasi-static lung compliance were largely unaffected by neutralization of IL-13 and/or IL-17A. However, neutralization of IL-13 alone or in combination with IL-17A significantly attenuated AHR and mucus metaplasia. Further, STAT6 activation was attenuated following IL-13 and IL-13/IL-17A Ab treatment. We next assessed the role of STAT6 in Th2/Th17-mediated allergic airway disease using STAT6(-/-) mice. STAT6(-/-) mice adoptively transferred with Th2/Th17 cells had decreased AHR compared with controls. These data suggest that IL-13 drives AHR and mucus metaplasia in a STAT6-dependent manner, without directly contributing to airway or tissue inflammation. IL-17A independently contributes to AHR, but it only partially mediates inflammation and mucus metaplasia in a mixed Th2/Th17 model of steroid-resistant asthma.

Indexed as

Adoptive TransferAnimalsAsthmaDisease Models, AnimalDrug ResistanceImmunoblottingInterleukin-13Interleukin-17MetaplasiaMiceMice, Inbred BALB CMice, KnockoutMice, SCIDMice, TransgenicMucusPolymerase Chain ReactionInterleukin-13Interleukin-17

Identifiers

PMID26729801
PMCPMC4724491
OpenAlexW2230330630

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.