Evidence map›Paper›PMID 24968337›Full record

ArticlePloS one2014

Concomitant exposure to ovalbumin and endotoxin augments airway inflammation but not airway hyperresponsiveness in a murine model of asthma.

John Mac Sharry, Karim H Shalaby, Cinzia Marchica, Soroor Farahnak, Tien Chieh-Li, Susan Lapthorne, Salman T Qureshi, Fergus Shanahan, James G Martin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Lung CD4Cell reports · 2025
    Article
  5. Article
  6. Article
  7. The Role of Heat Shock Protein 70 kDa in Asthma.Journal of asthma and allergy · 2020
    Review
  8. Lipopolysaccharide Exposure Alleviates Asthma in Mice by Regulating Th1/Th2 and Treg/Th17 Balance.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

9 authors at 4 institutions in 2 countries.

John Mac SharryAlimentary Pharmabiotic Centre, School of Medicine, University College Cork, National University of Ireland, Cork, Ireland.
Karim H ShalabyMeakins Christie Laboratories, Department of Medicine, McGill University, Montreal, Canada.
Cinzia MarchicaMeakins Christie Laboratories, Department of Medicine, McGill University, Montreal, Canada.
Soroor FarahnakMeakins Christie Laboratories, Department of Medicine, McGill University, Montreal, Canada.
Tien Chieh-LiMeakins Christie Laboratories, Department of Medicine, McGill University, Montreal, Canada.
Susan LapthorneAlimentary Pharmabiotic Centre, School of Medicine, University College Cork, National University of Ireland, Cork, Ireland.
Salman T QureshiMeakins Christie Laboratories, Department of Medicine, McGill University, Montreal, Canada.
Fergus ShanahanAlimentary Pharmabiotic Centre, School of Medicine, University College Cork, National University of Ireland, Cork, Ireland.
James G MartinMeakins Christie Laboratories, Department of Medicine, McGill University, Montreal, Canada.
Christie (Canada) · CAMcGill University · CANational University of Ireland · IEUniversity College Cork · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Varying concentrations of lipopolysaccharide (LPS) in ovalbumin (OVA) may influence the airway response to allergic sensitization and challenge. We assessed the contribution of LPS to allergic airway inflammatory responses following challenge with LPS-rich and LPS-free commercial OVA. BALB/c mice were sensitized with LPS-rich OVA and alum and then underwent challenge with the same OVA (10 µg intranasally) or an LPS-free OVA. Following challenge, bronchoalveolar lavage (BAL), airway responsiveness to methacholine and the lung regulatory T cell population (Treg) were assessed. Both OVA preparations induced BAL eosinophilia but LPS-rich OVA also evoked BAL neutrophilia. LPS-free OVA increased interleukin (IL)-2, IL-4 and IL-5 whereas LPS-rich OVA additionally increased IL-1β, IL-12, IFN-γ, TNF-α and KC. Both OVA-challenged groups developed airway hyperresponsiveness. TLR4-deficient mice challenged with either OVA preparation showed eosinophilia but not neutrophilia and had increased IL-5. Only LPS-rich OVA challenged mice had increased lung Tregs and LPS-rich OVA also induced in vitro Treg differentiation. LPS-rich OVA also induced a Th1 cytokine response in human peripheral blood mononuclear cells.We conclude that LPS-rich OVA evokes mixed Th1, Th2 and innate immune responses through the TLR-4 pathway, whereas LPS-free OVA evokes only a Th2 response. Contaminating LPS is not required for induction of airway hyperresponsiveness but amplifies the Th2 inflammatory response and is a critical mediator of the neutrophil, Th1 and T regulatory cell responses to OVA.

Indexed as

AnimalsAsthmaBronchoalveolar Lavage FluidCells, CulturedDrug SynergismEosinophilsHumansInflammationInterferon-gammaInterleukinsLipopolysaccharidesMaleMiceMice, Inbred BALB CNeutrophilsOvalbuminInterferon-gammaInterleukinsLipopolysaccharidesOvalbuminTumor Necrosis Factor-alpha

Identifiers

PMID24968337
PMCPMC4072597
OpenAlexW1982018053

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.