Evidence map›Paper›PMID 22984249›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012

Role of TNFR1 in the innate airway hyperresponsiveness of obese mice.

Ming Zhu, Alison S Williams, Lucas Chen, Allison P Wurmbrand, Erin S Williams, Stephanie A Shore

Open access · greenAbstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. A Review onEndocrine, metabolic & immune disorders drug targets · 2025
    Review
  2. Review
  3. Article
  4. Article
  5. Role of ROCK2 in CD4Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2017
    Article
  6. Mechanisms of Asthma in Obesity. Pleiotropic Aspects of Obesity Produce Distinct Asthma Phenotypes.American journal of respiratory cell and molecular biology · 2016
    Review
  7. Innate and ozone-induced airway hyperresponsiveness in obese mice: role of TNF-α.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  8. The impact of diet on asthma and allergic diseases.Nature reviews. Immunology · 2015
    Review
  9. Review
  10. Article
  11. Article
  12. 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

6 authors at 1 institution in 1 country.

Ming ZhuDepartment of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
Alison S Williams
Lucas Chen
Allison P Wurmbrand
Erin S Williams
Stephanie A Shore
Massachusetts Department of Public Health · US

Funding

Translational Research Support CoreP30ES000002 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI SUSAN A KORRICK · 1985 to 2026
$44.6M
Impact of Obesity on Airway Responses to Air PollutionR01ES013307 · NIEHS · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI SHORE, STEPHANIE A · 2005 to 2019
$5.2M
Obesity and Airway ResponsivenessR01HL084044 · NHLBI · HARVARD SCHOOL OF PUBLIC HEALTH · PI SHORE, STEPHANIE A · 2007 to 2011
$2.1M
NHLBI NIH HHS HL-084044NIEHS NIH HHS ES-00002NIEHS NIH HHS ES-013307NIEHS NIH HHS P30 ES000002
6 · The paper itself

Abstract

The purpose of this study was to examine the role of tumor necrosis factor receptor 1 (TNFR1) in the airway hyperresponsiveness characteristic of obese mice. Airway responsiveness to intravenous methacholine was measured using the forced oscillation technique in obese Cpe(fat) mice that were either sufficient or genetically deficient in TNFR1 (Cpe(fat) and Cpe(fat)/TNFR1(-/-) mice) and in lean mice that were either sufficient or genetically deficient in TNFR1 [wild-type (WT) and TNFR1(-/-) mice]. Compared with lean WT mice, Cpe(fat) mice exhibited airway hyperresponsiveness. Airway hyperresponsives was also greater in Cpe(fat)/TNFR1(-/-) than in Cpe(fat) mice. Compared with WT mice, Cpe(fat) mice had increases in bronchoalveolar lavage fluid concentrations of several inflammatory moieties including eotaxin, IL-9, IP-10, KC, MIG, and VEGF. These factors were also significantly elevated in Cpe(fat)/TNFR1(-/-) vs. TNFR1(-/-) mice. Additional moieties including IL-13 were also elevated in Cpe(fat)/TNFR1(-/-) vs. TNFR1(-/-) mice but not in Cpe(fat) vs. WT mice. IL-17A mRNA expression was greater in Cpe(fat)/TNFR1(-/-) vs. Cpe(fat) mice and in TNFR1(-/-) vs. WT mice. Analysis of serum indicated that obesity resulted in systemic as well as pulmonary inflammation, but TNFR1 deficiency had little effect on this systemic inflammation. Our results indicate that TNFR1 is protective against the airway hyperresponsiveness associated with obesity and suggest that effects on pulmonary inflammation may be contributing to this protection.

Indexed as

AnimalsAsthmaBronchial HyperreactivityBronchial Provocation TestsBronchoalveolar Lavage FluidDisease Models, AnimalHumansInflammation MediatorsInterleukin-17MiceMice, Inbred C57BLMice, KnockoutMice, ObeseObesityReceptors, Tumor Necrosis Factor, Type IRespiratory MechanicsInflammation MediatorsInterleukin-17Receptors, Tumor Necrosis Factor, Type IRNA, MessengerTnfrsf1a protein, mouse

Identifiers

PMID22984249
PMCPMC3524665
OpenAlexW2136276388

What OpenQuestion holds

Textmetadata
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.