Evidence map›Paper›PMID 23427255›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

The inflammatory twitch as a general strategy for controlling the host response.

Joshua J Pothen, Matthew E Poynter, Jason H T Bates

Abstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. 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
–field-weighted citation impact
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.

  1. Multi-scale models of lung fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
  2. Agent-based models of inflammation in translational systems biology: A decade later.Wiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
  3. Pathophysiology to Phenotype in the Asthma of Obesity.Annals of the American Thoracic Society · 2017
    Review
  4. Systems physiology of the airways in health and obstructive pulmonary disease.Wiley interdisciplinary reviews. Systems biology and medicine · 2016
    Review
  5. Mouse Modeling of Obese Lung Disease. Insights and Caveats.American journal of respiratory cell and molecular biology · 2016
    Review
  6. Dissecting the inflammatory twitch in allergically inflamed mice.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  7. Article
  8. A computational model of unresolved allergic inflammation in chronic asthma.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  9. Article
  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

3 authors.

Joshua J PothenDepartment of Medicine, University of Vermont College of Medicine, Burlington, VT 05405, USA.
Matthew E Poynter
Jason H T Bates

Funding

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
A multi-scale approach to airway hyperresponsiveness: from molecule to organR01HL103405 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI BATES, JASON HT, LAUZON, ANNE-MARIE · 2010 to 2013
$3.6M
Serum Amyloid A3 in Allergic Asthma: An Endogenous Mediator of Disease SeverityR01HL107291 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI POYNTER, MATTHEW E · 2012 to 2015
$1.5M
NHLBI NIH HHS R01 HL103405NHLBI NIH HHS R01 HL107291NHLBI NIH HHS T32 HL076122NIGMS NIH HHS P30 GM103532
6 · The paper itself

Abstract

Allergic inflammation is a general host-defense mechanism for dealing with perceived foreign invaders. Although most effort has been directed toward understanding how this response gets turned on, how it gets turned off again when no longer needed is just as important to an organism's survival. We postulate that the control of the allergic inflammatory response is achieved via frequency modulation whereby a sequence of self-resolving events is repetitively invoked only so long as Ag is present. This leads to the notion of a unitary inflammatory event that we argue has formal similarity to the skeletal muscle twitch, albeit manifest over a much longer time scale. To test the plausibility of this hypothesis, we created an agent-based computational model of the allergic inflammatory response in the lungs. Continual stimulation of the model results in cycles of tissue damage and repair interspersed with periods of nonresponsiveness indicative of a refractory period. These findings are consistent with the inflammatory twitch hypothesis and the notion that the allergic inflammatory response is controlled via frequency modulation. We speculate that chronic inflammatory diseases may represent a failure of the inflammatory twitch to resolve toward baseline.

Indexed as

Models, ImmunologicalAnimalsComputer SimulationHumansHypersensitivityInflammation

Identifiers

PMID23427255
PMCPMC3608740

What OpenQuestion holds

Textmetadata
LicenceTDM
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.