Evidence map›Paper›PMID 19901346›Full record

ArticleAmerican journal of respiratory cell and molecular biology2010

Neurotransmitters in airway parasympathetic neurons altered by neurotrophin-3 and repeated allergen challenge.

Jenny Pan, Holly K Rhode, Bradley J Undem, Allen C Myers

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2010. 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
0.5field-weighted citation impact, top 40% 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. Effect of BDNF on airway inflammation in a rat model of COPD.Experimental and therapeutic medicine · 2021
    Article
  3. Cholinergic neuroplasticity in asthma driven by TrkB signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  4. Airway Innervation and Plasticity in Asthma.Physiology (Bethesda, Md.) · 2019
    Review
  5. Mechanisms of organophosphorus pesticide toxicity in the context of airway hyperreactivity and asthma.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  6. The mode of action of anticholinergics in asthma.The European respiratory journal · 2018
    Review
  7. Article
  8. Neurotrophins in Asthma.Current allergy and asthma reports · 2018
    Review
  9. Article
  10. Brain-derived neurotrophic factor in the airways.Pharmacology & therapeutics · 2014
    Review
  11. Mechanisms underlying the neuronal-based symptoms of allergy.The Journal of allergy and clinical immunology · 2014
    Review
  12. Airway smooth muscle in airway reactivity and remodeling: what have we learned?American journal of physiology. Lung cellular and molecular physiology · 2013
    Review
  13. Synaptic and membrane properties of parasympathetic ganglionic neurons innervating mouse trachea and bronchi.American journal of physiology. Lung cellular and molecular physiology · 2010
    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

4 authors at 1 institution in 1 country.

Jenny PanDivision of Allergy and Clinical Immunology, the Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
Holly K Rhode
Bradley J Undem
Allen C Myers
Johns Hopkins University · US

Funding

MAST CELL-NERVE INTERACTIONS IN AIRWAYSR01HL038095 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI UNDEM, BRADLEY JOEL · 1993 to 2010
$2.9M
Neurotrophin Regulation of the Airway Parasympathetic Nervous SystemR01HL088608 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MYERS, ALLEN C · 2008 to 2011
$1.7M
THE INTERACTIONS BETWEEN MAST CELLS &NERVES IN AIRWAYSR29HL038095 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI UNDEM, BRADLEY J · 1988 to 1992
–
NHLBI NIH HHS HL038095NHLBI NIH HHS HL088608
6 · The paper itself

Abstract

Changes in airway nerves associated with chronic inflammation may underlie the pathogenesis and symptoms of lower airway diseases, such as asthma. The molecules most likely causing such alterations are neurotrophins (NTs) and/or related neurokines. In several species, including humans, lower airway parasympathetic postganglionic neurons that project axons to airway smooth muscle are either cholinergic or nonadrenergic noncholinergic (NANC), the latter synthesizing vasoactive intestinal peptide and nitric oxide, but not acetylcholine. In guinea pig trachealis smooth muscle, cholinergic nerve terminals arise from ganglionic neurons located near the tracheal smooth muscle, whereas the source of NANC nerve fibers is from neurons in ganglia located in the adjacent myenteric plexus of the esophagus, making this an ideal species to study regulation of parasympathetic neurotransmitter phenotypes. In the present study, we determined that, 48 hours after repeated allergen challenge, the NANC phenotype of airway parasympathetic ganglionic neurons changed to a cholinergic phenotype, and NT-3 mimicked this change. Nerve growth factor, brain-derived neurotrophic factor, leukemia inhibitory factor, or IL-1β had no effect on either phenotype, and they did not induce these neurons to synthesize substance P or tyrosine hydroxylase. These results indicate a role for inflammation and NT-3 in regulating biochemical and anatomical characteristics of principal neurons in adult airway parasympathetic ganglia.

Indexed as

AllergensAnimalsEsophagusFluorescent Antibody TechniqueFrozen SectionsGuinea PigsLungMaleNeuronsNeurotransmitter AgentsNeurotrophin 3Parasympathetic Nervous SystemPneumoniaAllergensNeurotransmitter AgentsNeurotrophin 3

Identifiers

PMID19901346
PMCPMC2951875
OpenAlexW2122033688

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.