Evidence map›Paper›PMID 22074702›Full record

ArticleAmerican journal of respiratory cell and molecular biology2012

Inhibition of Pim1 kinase activation attenuates allergen-induced airway hyperresponsiveness and inflammation.

Yoo Seob Shin, Katsuyuki Takeda, Yoshiki Shiraishi, Yi Jia, Meiqin Wang, Leila Jackson, A Dale Wright, Laura Carter, John Robinson, Erik Hicken and 1 more

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The role of Pim-1 kinases in inflammatory signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  5. Review
  6. Article
  7. The Role of NLRP3 Inflammasome in Lupus Nephritis.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Role of PIM2 in allergic asthma.Molecular medicine reports · 2017
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

11 authors at 2 institutions in 1 country.

Yoo Seob ShinDivision of Cell Biology, Department of Pediatrics, National Jewish Health, Denver, CO 80206, USA.
Katsuyuki Takeda
Yoshiki Shiraishi
Yi Jia
Meiqin Wang
Leila Jackson
A Dale Wright
Laura Carter
John Robinson
Erik Hicken
Erwin W Gelfand
National Jewish Health · USArray BioPharma (United States) · US

Funding

Signaling Memory in Chronic AsthmaP01HL036577 · NHLBI · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 1986 to 2011
$18.7M
Naturally Occurring T Regulatory Cells Control Airway HyperresponsivenessR01AI077609 · NIAID · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 2009 to 2013
$2.3M
Naturally occurring T regulatory cells control airway hyperresponsivenessR56AI077609 · NIAID · NATIONAL JEWISH HEALTH · PI GELFAND, ERWIN WILLIAM · 2008 to 2008
$487k
NHLBI NIH HHS HL-36577NHLBI NIH HHS P01 HL036577NIAID NIH HHS AI-77609NIAID NIH HHS R01 AI077609NIAID NIH HHS R56 AI077609
6 · The paper itself

Abstract

Pim kinases are a family of serine/threonine kinases whose activity can be induced by cytokines involved in allergy and asthma. These kinases play a role in cell survival and proliferation, but have not been examined, to the best of our knowledge, in the development of allergic disease. This study sought to determine the role of Pim1 kinase in the development of allergic airway responses. Mice were sensitized and challenged with antigen (primary challenge), or were sensitized, challenged, and rechallenged with allergen in a secondary model. To assess the role of Pim1 kinase, a small molecule inhibitor was administered orally after sensitization and during the challenge phase. Airway responsiveness to inhaled methacholine, airway and lung inflammation, cell composition, and cytokine concentrations were assessed. Lung Pim1 kinase concentrations were increased after ovalbumin sensitization and challenge. In the primary allergen challenge model, treatment with the Pim1 kinase inhibitor after sensitization and during airway challenges prevented the development of airway hyperresponsiveness, eosinophilic airway inflammation, and goblet cell metaplasia, and increased Th2 cytokine concentrations in bronchoalveolar fluid in a dose-dependent manner. These effects were also demonstrated after a secondary allergen challenge, where lung allergic disease was established before treatment. After treatment with the inhibitor, a significant reduction was evident in the number of CD4(+) and CD8(+) T cells and concentrations of cytokines in the airways. The inhibition of Pim1 kinase was effective in preventing the development of airway hyperresponsiveness, airway inflammation, and cytokine production in allergen-sensitized and allergen-challenged mice. These data identify the important role of Pim1 kinase in the full development of allergen-induced airway responses.

Indexed as

AllergensAnimalsBronchoalveolar Lavage FluidCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesDisease Models, AnimalEnzyme InhibitorsFemaleGoblet CellsHypersensitivityInflammationLungMethacholine ChlorideMiceMice, Inbred BALB CAllergensCytokinesEnzyme InhibitorsMethacholine ChlorideOvalbuminPim1 protein, mouseProto-Oncogene Proteins c-pim-1

Identifiers

PMID22074702
PMCPMC3359953
OpenAlexW1997249897

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.