Evidence map›Paper›PMID 27064658›Full record

ArticleAmerican journal of respiratory cell and molecular biology2016

Weight Loss Decreases Inherent and Allergic Methacholine Hyperresponsiveness in Mouse Models of Diet-Induced Obese Asthma.

Jennifer L Ather, Michael Chung, Laura R Hoyt, Matthew J Randall, Anna Georgsdottir, Nirav A Daphtary, Minara I Aliyeva, Benjamin T Suratt, Jason H T Bates, Charles G Irvin and 4 more

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

  1. Effect of obesity on sinonasal disease in asthma.The Journal of asthma : official journal of the Association for the Care of Asthma · 2018
    Trial
  2. Review
  3. Article
  4. Mitoquinone mesylate attenuates pathological features of lean and obese allergic asthma in mice.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  5. Diet-induced obesity worsens allergen-induced type 2/type 17 inflammation in airways by enhancing DUOX1 activation.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  6. Article
  7. Article
  8. Therapeutic ketosis decreases methacholine hyperresponsiveness in mouse models of inherent obese asthma.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  9. Review
  10. Article
  11. Obese adipose tissue modulates proinflammatory responses of mouse airway epithelial cells.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Eosinophilic and Noneosinophilic Asthma.American journal of respiratory and critical care medicine · 2018
    Review
  17. Asthma and Obesity: The Chicken, the Egg, or More Than One Beast?American journal of respiratory and critical care medicine · 2017
    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

14 authors at 1 institution in 1 country.

Jennifer L Ather1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Michael Chung1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Laura R Hoyt1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Matthew J Randall1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Anna Georgsdottir1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Nirav A Daphtary1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Minara I Aliyeva1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Benjamin T Suratt1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Jason H T Bates1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Charles G Irvin1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Sheila R Russell2 Department of Surgery, University of Vermont, Burlington, Vermont.
Patrick M Forgione2 Department of Surgery, University of Vermont, Burlington, Vermont.
Anne E Dixon1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
Matthew E Poynter1 Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, and.
University of Vermont · US

Funding

Vermont Immunobioloigy/ Infectious Diseases CenterP20GM103496 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2012 to 2015
$8.7M
Vermont Immunology/Infectious Diseases CenterP30GM118228 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2016 to 2021
$6.8M
Multidisciplinary Training in Lung BiologyT32HL076122 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI IRVIN, CHARLES G, POYNTER, MATTHEW E · 2004 to 2023
$6.1M
Translational Research in Lung Biology and DiseaseP30GM103532 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI IRVIN, CHARLES G · 2012 to 2016
$3.7M
NHLBI NIH HHS T32 HL076122NIGMS NIH HHS P20 GM103496NIGMS NIH HHS P30 GM103532NIGMS NIH HHS P30 GM118228
6 · The paper itself

Abstract

Obese asthma presents with inherent hyperresponsiveness to methacholine or augmented allergen-driven allergic asthma, with an even greater magnitude of methacholine hyperresponsiveness. These physiologic parameters and accompanying obese asthma symptoms can be reduced by successful weight loss, yet the underlying mechanisms remain incompletely understood. We implemented mouse models of diet-induced obesity, dietary and surgical weight loss, and environmental allergen exposure to examine the mechanisms and mediators of inherent and allergic obese asthma. We report that the methacholine hyperresponsiveness in these models of inherent obese asthma and obese allergic asthma manifests in distinct anatomical compartments but that both are amenable to interventions that induce substantial weight loss. The inherent obese asthma phenotype, with characteristic increases in distal airspace tissue resistance and tissue elastance, is associated with elevated proinflammatory cytokines that are reduced with dietary weight loss. Surprisingly, bariatric surgery-induced weight loss further elevates these cytokines while reducing methacholine responsiveness to levels similar to those in lean mice or in formerly obese mice rendered lean through dietary intervention. In contrast, the obese allergic asthma phenotype, with characteristic increases in central airway resistance, is not associated with increased adaptive immune responses, yet diet-induced weight loss reduces methacholine hyperresponsiveness without altering immunological variables. Diet-induced weight loss is effective in models of both inherent and allergic obese asthma, and our examination of the fecal microbiome revealed that the obesogenic Firmicutes/Bacteroidetes ratio was normalized after diet-induced weight loss. Our results suggest that structural, immunological, and microbiological factors contribute to the manifold presentations of obese asthma.

Indexed as

Weight LossAnimalsAsthmaBacteriaBariatric SurgeryBronchial HyperreactivityCytokinesDietDisease Models, AnimalHypersensitivityInflammation MediatorsIntestinesMaleMethacholine ChlorideMice, Inbred C57BLMice, ObeseCytokinesInflammation MediatorsMethacholine Chlorideairway hyperresponsivenessasthmabariatric surgeryobesityweight loss

Identifiers

PMID27064658
PMCPMC4979374
OpenAlexW2319514641

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.