Evidence map›Paper›PMID 24484440›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Persistence of serotonergic enhancement of airway response in a model of childhood asthma.

Brian D Moore, Dallas M Hyde, Lisa A Miller, Emily M Wong, Edward S Schelegle

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Newly divided eosinophils limit ozone-induced airway hyperreactivity in nonsensitized guinea pigs.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  9. Review
  10. 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

5 authors at 3 institutions in 2 countries.

Brian D Moore1 University of the Pacific, Stockton, California; and.
Dallas M Hyde
Lisa A Miller
Emily M Wong
Edward S Schelegle
Institute of Cell Biology and Neurobiology · ITUniversity of California, Davis · USUniversity of the Pacific · US

Funding

National Institute on Aging (NIA) ColonyP51OD011107 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Simon J. Atkinson · 2012 to 2026
$191.5M
ROLE OF EPITHELIAL CELLS IN OZONE-NITROGEN DIOXIDE INTERACTIONP01ES000628 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HYDE, DALLAS MELVIN · 1985 to 2010
$12.5M
NIEHS NIH HHS P01 ES000628NIEHS NIH HHS P01ES000628-33NIH HHS P51 OD011107
6 · The paper itself

Abstract

The persistence of airway hyperresponsiveness (AHR) and serotonergic enhancement of airway smooth muscle (ASM) contraction induced by ozone (O3) plus allergen has not been evaluated. If this mechanism persists after a prolonged recovery, it would indicate that early-life exposure to O3 plus allergen induces functional changes predisposing allergic individuals to asthma-related symptoms throughout life, even in the absence of environmental insult. A persistent serotonergic mechanism in asthma exacerbations may offer a novel therapeutic target, widening treatment options for patients with asthma. The objective of this study was to determine if previously documented AHR and serotonin-enhanced ASM contraction in allergic monkeys exposed to O3 plus house dust mite allergen (HDMA) persist after prolonged recovery. Infant rhesus monkeys sensitized to HDMA were exposed to filtered air (FA) (n = 6) or HDMA plus O3 (n = 6) for 5 months. Monkeys were then housed in a FA environment for 30 months. At 3 years, airway responsiveness was assessed. Airway rings were then harvested, and ASM contraction was evaluated using electrical field stimulation with and without exogenous serotonin and serotonin-subtype receptor antagonists. Animals exposed to O3 plus HDMA exhibited persistent AHR. Serotonin exacerbated the ASM contraction in the exposure group but not in the FA group. Serotonin subtype receptors 2, 3, and 4 appear to drive the response. Our study shows that AHR and serotonin-dependent exacerbation of cholinergic-mediated ASM contraction induced by early-life exposure to O3 plus allergen persist for at least 2.5 years and may contribute to a persistent asthma phenotype.

Indexed as

Disease Models, AnimalAllergensAnimalsAntigens, DermatophagoidesAsthmaChildDisease ProgressionHumansMacaca mulattaMuscle ContractionRespiratory HypersensitivityRespiratory SystemSerotoninSerotonin Receptor AgonistsAllergensAntigens, DermatophagoidesSerotoninSerotonin Receptor AgonistsantigenshyperresponsivenessMacaca mulattaozoneserotonin

Identifiers

PMID24484440
PMCPMC4091858
OpenAlexW2068504631

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.