Evidence map›Paper›PMID 14623911›Full record

ArticleThe Journal of experimental medicine2003

Blockade of inflammation and airway hyperresponsiveness in immune-sensitized mice by dominant-negative phosphoinositide 3-kinase-TAT.

Shigeharu Myou, Alan R Leff, Saori Myo, Evan Boetticher, Jiankun Tong, Angelo Y Meliton, Jie Liu, Nilda M Munoz, Xiangdong Zhu

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

122 citing papers in PubMed, 259 citations in OpenAlex.

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  14. Therapeutic effects of a combination ofFrontiers in nutrition · 2025
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  16. Photobiomodulation Mitigates PMAntioxidants (Basel, Switzerland) · 2024
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  20. Unleashing AdipoRon's Potential: A Fresh Approach to TackleJournal of inflammation research · 2024
    Article

62 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Shigeharu MyouSection of Pulmonary and Critical Care Medicine, Department of Medicine, The University of Chicago, 5841 South Maryland Avenue, Chicago, IL 60637, USA.
Alan R Leff
Saori Myo
Evan Boetticher
Jiankun Tong
Angelo Y Meliton
Jie Liu
Nilda M Munoz
Xiangdong Zhu
Pulmonary and Critical Care Associates · USUniversity of Chicago · US

Funding

T CELL CO-STIMULATION IN ALLERGIC ASTHMAP50HL056399 · NHLBI · UNIVERSITY OF CHICAGO · PI WHITE, STEVEN R · 1996 to 2005
$9.1M
MECHANISMS OF AIRWAY HYPERRESPONSIVENESSR01HL046368 · NHLBI · UNIVERSITY OF CHICAGO · PI LEFF, ALAN RICHARD · 1991 to 2005
$1.7M
Mechanisms of Eosinophil AdhesionK08AI052109 · NIAID · UNIVERSITY OF CHICAGO · PI ZHU, XIANGDONG · 2002 to 2006
$429k
NHLBI NIH HHS HL-46368NHLBI NIH HHS HL-56399NHLBI NIH HHS P50 HL056399NHLBI NIH HHS R01 HL046368NIAID NIH HHS AI-52109NIAID NIH HHS K08 AI052109
6 · The paper itself

Abstract

Phosphoinositide 3-kinase (PI3K) is thought to contribute to the pathogenesis of asthma by effecting the recruitment, activation, and apoptosis of inflammatory cells. We examined the role of class IA PI3K in antigen-induced airway inflammation and hyperresponsiveness by i.p. administration into mice of Deltap85 protein, a dominant negative form of the class IA PI3K regulatory subunit, p85alpha, which was fused to HIV-TAT (TAT-Deltap85). Intraperitoneal administration of TAT-Deltap85 caused time-dependent transduction into blood leukocytes, and inhibited activated phosphorylation of protein kinase B (PKB), a downstream target of PI3K, in lung tissues in mice receiving intranasal FMLP. Antigen challenge elicited pulmonary infiltration of lymphocytes, eosinophils and neutrophils, increase in mucus-containing epithelial cells, and airway hyperresponsiveness to methacholine. Except for modest airway neutrophilia, these effects all were blocked by treatment with 3-10 mg/kg of TAT-Deltap85. There was also significant reduction in IL-5 and IL-4 secretion into the BAL. Intranasal administration of IL-5 caused eosinophil migration into the airway lumen, which was attenuated by systemic pretreatment with TAT-Deltap85. We conclude that PI3K has a regulatory role in Th2-cell cytokine secretion, airway inflammation, and airway hyperresponsiveness in mice.

Indexed as

AnimalsHypersensitivityInflammationInterleukin-5LungMicePhosphatidylinositol 3-KinasesRespiratory Tract DiseasesInterleukin-5Phosphatidylinositol 3-Kinases

Identifiers

PMID14623911
PMCPMC2194122
OpenAlexW2135418193

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.